<?xml version="1.0" encoding="utf-8"?>
			<journal>
			<title>Avicenna Journal of Phytomedicine</title>
			<title_fa></title_fa>
			<short_title></short_title>
			<subject>Medical Sciences</subject>
			<web_url>https://ajp.mums.ac.ir/</web_url>
			<journal_hbi_system_id>0</journal_hbi_system_id>
			<journal_hbi_system_user></journal_hbi_system_user>
			<journal_id_issn>2228-7930</journal_id_issn>
			<journal_id_issn_online>2228-7949</journal_id_issn_online>
			<journal_id_pii></journal_id_pii>
			<journal_id_doi></journal_id_doi>
			<journal_id_iranmedex></journal_id_iranmedex>
			<journal_id_magiran></journal_id_magiran>
			<journal_id_sid></journal_id_sid>
			<journal_id_nlai></journal_id_nlai>
			<journal_id_science></journal_id_science>
			<language>en</language>
			<pubdate>
				<type>jalali</type>
				<year>0</year>
				<month>0</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2023</year>
				<month>1</month>
				<day>1</day>
			</pubdate>
			<volume>13</volume>
			<number>1</number>
			<publish_type>online</publish_type>
			<publish_edition>1</publish_edition>
			<article_type>fulltext</article_type>
			<articleset><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Letter to Editor on: "Ginger (Zingiber officinale roscoe) extract could upregulate the renal expression of NRF2 and TNFα and prevents ethanol-induced toxicity in rat kidney" by Akbari et al.</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Letter to Editor</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[A recent study entitled “Ginger(Zingiber officinale roscoe) extractcould upregulate the renal expressionof Nrf2 and TNFα and preventsethanol-induced toxicity in rat kidney”that was published in this journal byFathi et al., 2021) states that ethanolcan activate Nrf2 expression. Nuclearfactor E2-related factor (Nrf2)regulates the expression of a variety ofgenes responsible for intracellulardetoxification, and antioxidant, antiinflammation, anti-stress activities, etc(Ezhilarasan et al., 2016). Nrf2 iscrucial for the induction of endogenousantioxidant enzymes such as hemeoxygenase 1 and reduced glutathionevia activation of intracellular antioxidantresponsive element. Therefore, activationof Nrf2 pathway by phytochemicals has beendemonstrated to provide protection againstalcohol-related abnormalities suggesting thebeneficial role of Nrf2 activation (Zhao etal., 2018; Ezhilarasan et al., 2016). Besides,a growing body of evidence reports theprotective role of Nrf2 against a number ofkidney diseases (Hejazian et al., 2021). Nrf2activates several intracellular antioxidantenzymes during the onset of intracellularoxidative stress (Ezhilarasan, 2018).Therefore, Nrf-2 activation is usuallyconsidered to have a beneficial effect.Previous studies also showed that ethanoladministrations can downregulate orsuppress Nrf-2 expression (Sueblinvong etal., 2014; Shanmugam et al., 2019). In viewof the above scenario, as a powerfuloxidative agent, how ethanol could activateNrf2 expression? The authors have showedthat ginger, ethanol and ethanol+gingertreatments can activate Nrf2 expression. Themanuscript was also failed to discuss aboutthe reason behind Nrf2 upregulation afterethanol administration. These discrepanciesmust be addressed in the discussion part.The objectives of the study wereinteresting, however, there were somediscrepancies in the title and their resultsfurnished. Therefore, we wish to seek yourattention towards this publication. The mainconcern of this publication is the title. Thetitle says “Ginger (Zingiber officinaleElumalai et al. AJP, Vol. 13, No. 1, Jan-Feb 2023 2roscoe) extract could upregulate therenal expression of Nrf-2 and tumornecrosis factor alpha (TNF-α) andprevents ethanol-induced toxicity in ratkidney”. However, in results theauthors were reported that Ginger candownregulate ethanol-induced TNF-α.Moreover, as reported in the title Gingerextract did not ameliorate ethanol-inducedNrf-2 downregulation. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Zingiber officinale, ginger, Ethanol, Nuclear factor E2-related factor</keyword>
				<start_page>1</start_page>
				<end_page>2</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21187.html</web_url>
			<author_list><author>
				<first_name>Perumal</first_name>
				<middle_name></middle_name>
				<last_name>Elumalai</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>elusandy@gmail.com</email>
				<code>91745</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, The Gold lab, Molecular Medicine and Toxicology Division, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, Tamil Nadu, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Devaraj</first_name>
				<middle_name></middle_name>
				<last_name>Ezhilarasan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ezhild@gmail.com</email>
				<code>91744</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacology, The Gold lab, Molecular Medicine and Toxicology Division, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, Tamil Nadu, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Subramanian</first_name>
				<middle_name></middle_name>
				<last_name>Raghunandhakumar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>raghunandhakumar@gmail.com</email>
				<code>91746</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, The Gold lab, Molecular Medicine and Toxicology Division, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, Tamil Nadu, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Reply to Letter to Editor by Elumalai et al. re : "Ginger (Zingiber officinale roscoe) extract could upregulate the renal expression of NRF2 and TNFα and prevents ethanol-induced toxicity in rat kidney"</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Letter to Editor</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Thanks for your valuable commenton the article entitled: “Ginger(Zingiber officinale roscoe) extractcould upregulate the renal expressionof NRF2 and TNFα and preventsethanol-induced toxicity in rat kidney”.We reviewed your comment. In thebeginning, I think it is necessary tofirst give an overview of NRF2 and itsexpression.Nuclear factor erythroid 2–relatedfactor 2 (Nrf2) is a transcription factorthat regulates important antioxidantand phase II detoxification genesagainst oxidative stress (Tonelli et al.,2017). Nrf2 is involved in theregulation of (1) production,utilization, and regeneration ofglutathione (GSH) and thioredoxin (TXN),(2) nicotinamide adenine dinucleotidephosphate (NADPH) regeneration, (3) hemeand iron metabolism, (4) reactive oxygenspecies (ROS) and xenobiotic detoxification(Tonelli et al., 2017). Nrf2 activity issubjected to regulation at various levelsincluding protein stability, transcription, andpost-transcription (Tonelli et al., 2017; Li etal., 2019). Regulation of Nrf2 proteinstability level occurs mainly by keap-1-dependent and keap-1-independentpathways. In addition to the modulation ofNrf2 protein stability, regulation of Nrf2signaling occurs at the transcriptional level.The transcriptional factors involved includethe aryl hydrocarbon receptor (AhR), NFκB, and Nrf2 itself (Li et al., 2019). Thetranscription of the Nrf2 gene is found to beactivated by AhR (Li et al., 2019), and theexpression of AhR may be decreased byethanol (Zhang et al., 2012). Nrf2 genepromoter also contains a binding site for NFκB, and NF-κB subunits p50 and p65 inducetransactivation of the Nrf2 gene (Rushworthet al., 2012). This explains the activation ofNrf2 by NF-κB-activating inflammatorycytokines. Although NF-κB activates Nrf2,Nrf2 activation attenuates NF-κB signaling,suggesting a cross-talk between Nrf2 andNF-κB (Cuadrado et al., 2014). Inhibition ofNF-κB signaling by Nrf2 may contribute, atleast partly, to the anti-inflammatoryfunction of Nrf2 activators, such assulforaphane (Sun et al., 2015). How Nrf2suppresses NF-κB signaling remainsAkbari AJP, Vol. 13, No. 1, Jan-Feb 2023 4unknown. It is suggested that Nrf2activation may shift the cellular redoxstatus to a more reducing state due toincreased expression of antioxidants(Li et al., 2019), and we know thatethanol or its metabolic products maydisrupt these conditions by producingdifferent species of free radicals(Comporti et al., 2010). Nrf2autoregulation is another mechanismthat regulates the transcription of thisgene. Due to the presence of ARE-likesequences in the promoter region ofthe Nrf2 gene, Nrf2 may activate itsown gene expression, leading toincreased production of Nrf2 protein(Kwak et al., 2002). This represents apositive feedback mechanism. On theother hand, Nrf2 may stimulate Keap1gene expression for its owndegradation (Lee et al., 2007). Thisnegative feedback is a mechanism tocontrol the undue expression of Nrf2and uncontrolled Nrf2 signaling (Leeet al., 2007). In fact, these descriptionsshow that the expression of this genecan be controlled by different andinterconnected cellular mechanismsthat are involved in variouspathophysiological events (Tebay etal., 2015; Wu et al., 2012). In vivo andin vitro studies showed thatinterventions such as ethanolconsumption (Wu et al., 2012, Gongand Cederbaum, 2006a, Dong et al.,2008), smoking (Knörr-Wittmann etal., 2005), or exposure to heavy metals(He et al., 2007; Korashy and El-Kadi,2006) have led to different changes inthe expression of this gene. Theexamination of each of these studiesshows contradictory results regardingthe expression of this gene, similar toour study. In addition, we were aware,based on studies by other researchersand previous studies on the expressionof this gene that the results presentedin our article may have occurredcontrary to what has been expected sofar. Nevertheless, we reported what weachieved. In addition, it should be noted thatdespite the results of all in vivo and in vivostudies, we face a complex and dynamicbiological system in the face of harmfulinterventions that can individually produceadaptations and compensatory responses,and conflicting results that justify manyunexpected data. Therefore, reporting aresult in a study that is different from otherstudies is not far from the mind and isusually seen in many studies in differentfields.To answer to the question “why theexpression of this gene is increased in thepresence of ethanol? Despite the hypothesesthat exist in this field”, we have not yetencountered a study that has been conductedspecifically for this purpose. However, Gonget al. (2006) reported that the induction ofCYP2E1 by ethanol is one pathway throughwhich, ethanol generates oxidative stress.They also suggested that the levels of proteinand mRNA Nrf2 are increased whenCYP2E1 is elevated, and Nrf2 plays a keyrole in the adaptive response againstincreased oxidative stress caused byCYP2E1 (Gong and Cederbaum, 2006a).Dong et al. (2008) also reported thatmaternal ethanol treatment increased bothNrf2 protein levels and Nrf2-ARE binding inmouse embryos. It has also resulted in amoderate increase in the mRNA expressionof Nrf2 downstream target genes (Dong etal., 2008). Because exposure to ethanolresults in the generation of ROS which areknown to activate Nrf2 (Kensler et al.,2007), the observed Nrf2 activation wasexpected. This response is not unique toethanol-exposed embryos. Similar effectshave been observed in cells treated with anumber of other toxic chemicals, includingheavy metals (He et al., 2007; Korashy andEl-Kadi, 2006), cigarette smoke (KnörrWittmann et al., 2005), and arachidonic acid(Gong and Cederbaum, 2006b). Of particularinterest to this study is that an increase inNrf2 protein has also been observed in liversand hepatocytes of alcohol-fed mice and rats(Gong and Cederbaum, 2006a).Ginger, ethanol and renal NRF2 expressionAJP, Vol. 13, No. 1, Jan-Feb 2023 5However, another contradiction thatcan be seen in the results of this studyis the decrease in the activity ofantioxidant enzymes despite the highlevel of expression of the Nrf2 gene.These results can be easily describedand interpreted. A decrease in theactivity of antioxidant enzymes isactually due to their use to scavenge freeradicals produced due to incomplete ethanolmetabolism and the increase in theexpression of the Nrf2s gene actuallyindicates a compensatory response toimprove the response capacity of theantioxidant system and increase the activityof these enzymes]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>ginger, Ethanol, Kidney</keyword>
				<start_page>3</start_page>
				<end_page>6</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21188.html</web_url>
			<author_list><author>
				<first_name>Abolfazl</first_name>
				<middle_name></middle_name>
				<last_name>Akbari</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>akbariabolfazl@gmail.com</email>
				<code>91747</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Protective effects of hydroalcoholic extract of Rosa canina L. fruit on cyclophosphamide-induced testicular toxicity in mice</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Short communication</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Cyclophosphamide (CP)-induced testicular toxicity has been reported in recipient patients. The current study was designed to evaluate protective effects of hydroalcoholic extract of Rosa canina L. fruit (HARF) against CP-induced testicular toxicity in BALB/c mice.Materials and Methods: Thirty-five mice were divided into five groups as follows: group I (control), group II (CP, received CP 100 mg/kg on days 1, 8, 15, and 22), group III (CP + HARF 250 mg/kg), group IV (CP + HARF 500 mg/kg), and group V (CP + HARF 750 mg/kg). In the groups III, IV, and V that received CP, the HARF was simultaneously administered via intraperitoneal injections for 28 consecutive days starting from day 1. On the 29th day, sperm parameters, stress oxidative biomarkers, and mRNA expression of nuclear factor erythroid-derived-2 (Nrf2) in testis tissue, as well as blood testosterone were evaluated.Results: The CP exposure decreased sperm parameters, superoxide dismutase (SOD) activity, testosterone, and Nrf2 mRNA expression levels and increased the malondialdehyde (MDA). HARF at the dose of 500 mg/kg improved sperm count and viability and increased SOD and catalase activities, glutathione peroxidase (GPx) activity, testosterone level, and Nrf2 expression and reduced MDA. Also, HARF at the dose of 750 mg/kg improved sperm parameters and increased SOD, catalase, and GPx activities, total testosterone level, and Nrf2 expression, and reduced MDA in comparison with the CP group.Conclusion: According to our findings, HARF at the doses of 500 and 750 mg/kg inhibited the ruinous effects of CP on the reproductive system in mice.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Rosa canina L, Cyclophosphamide, Oxidative stress, Nuclear factor erythroid-derived-2, Sperm, Testosterone</keyword>
				<start_page>7</start_page>
				<end_page>17</end_page>
				<web_url>https://ajp.mums.ac.ir/article_20893.html</web_url>
			<author_list><author>
				<first_name>Rahmatollah</first_name>
				<middle_name></middle_name>
				<last_name>Parandin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rparandin@gmail.com</email>
				<code>90401</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biology, Payame Noor University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahnaz</first_name>
				<middle_name></middle_name>
				<last_name>Ghowsi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ghowsi.mahnaz@gmail.com</email>
				<code>90402</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Faculty of Sciences, Razi University, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ahmad</first_name>
				<middle_name></middle_name>
				<last_name>Dadbod</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ahmaddadbod@gmail.com</email>
				<code>90403</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Forensic Medicine, Judicature, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Nigella sativa supplementation and non-alcoholic fatty liver disease: A systematic review of clinical trials</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Review Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Based on the results of previous studies, the effects of N. sativa on some of the non-alcoholic fatty liver disease&#039;s (NAFLD) biomarkers were positive; however, there were conflicting results regarding other variables. Therefore, the present systematic review of clinical trials was designed to clarify whether N. sativa effectively prevents the progression of NAFLD.Materials and Methods: A search of four databases (Scopus, PubMed, Medline, and Google scholar) was conducted to identify the clinical trials that assessed the effects of N. sativa supplementation on NAFLD. The outcome variables of interest were biomarkers of hepatic steatosis, liver enzymes, insulin resistance, and inflammation.Results: Overall, four randomized clinical trials (RCTs) were included. In three studies, hepatic steatosis grade decreased significantly after N. sativa supplementation. Serum levels of liver enzymes reduced significantly in three of four included trials. In the only study that examined the effect of N. sativa on insulin resistance parameters, all variables related to this factor were significantly reduced. In two included studies that measured biomarkers of inflammation, the serum levels of tumor necrosis factor α (TNF-α), high-sensitive C-reactive protein (hs-CRP), and interleukin 6 (IL-6) decreased significantly after intaking N. sativa supplements.Conclusion: Although the efficacy of N. sativa on liver enzymes and the grade of hepatic steatosis was reported in some of the included studies, more well-designed clinical trials are needed to determine the definitive effects of N. sativa on NAFLD. The present study provides suggestions that help to design future studies in this field.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Nigella Sativa, Non-alcoholic fatty liver disease, Clinical Trials, Systematic review</keyword>
				<start_page>18</start_page>
				<end_page>33</end_page>
				<web_url>https://ajp.mums.ac.ir/article_20060.html</web_url>
			<author_list><author>
				<first_name>Abbas</first_name>
				<middle_name></middle_name>
				<last_name>Mohtashamian</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohammad_mhn_96@yahoo.com</email>
				<code>86658</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Biochemistry and Nutrition in Metabolic Diseases, Basic Science Research Institute, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Armin</first_name>
				<middle_name></middle_name>
				<last_name>Ebrahimzadeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>armin.ebrahimzadeh@yahoo.com</email>
				<code>86659</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Biochemistry and Nutrition in Metabolic Diseases, Basic Science Research Institute, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Shamekhi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>z_shamekhi2007@yahoo.com</email>
				<code>86660</code>
				<coreauthor>No</coreauthor>
				<affiliation>Sepidan Bagherololoom Higher Education College, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nasrin</first_name>
				<middle_name></middle_name>
				<last_name>Sharifi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sharifi-na@kaums.ac.ir</email>
				<code>86661</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Research Center for Biochemistry and Nutrition in Metabolic Diseases, Basic Science Research Institute, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Antidiabetic effects of Eryngium billardieri hydrosol in the treatment of type 2 diabetic patients: A double-blind randomized clinical trial</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Medicinal plants with fewer side effects and low cost than synthetic medicines are increasingly advised to treat diseases. The present study aimed to identify Eryngium billardieri compounds and evaluate the plant’s effects on hyperglycemic and hyperlipidemia indices, and liver, and kidney function.Materials and Methods: Following identification of Eryngium billardieri using GC/MS method, 72 participants were randomly divided into two groups (n=36 per group), receiving oral hypoglycemic medication (metformin) with or without 50 ml hydrosol  twice a day for three months as intervention and placebo control, respectively. Body mass index (BMI), systolic and diastolic blood pressure, fasting blood sugar (FBS), glycosylated hemoglobin (HbA1c), total cholesterol, triglyceride, HDL-C, and LDL-C levels were measured at the beginning and end of the experiment. Also, aspartate transaminase, alanine transaminase, blood urea nitrogen, and creatinine levels were measured to assess adverse effects on liver and kidney functions. Results: The main components were terpenes with 46.69% of the total ingredients of E. billardieri essential oil. Other prominent compounds identified included octanoic acid (12.14 %) and isoxazole (6.72 %).  Intergroup changes in blood parameters showed that E. billardieri hydrosol for three months could significantly reduce HbA1C and blood cholesterol levels but did not affect other measured parameters. Also, there were no adverse effects on kidney or liver function. Conclusion: The present findings showed that the consumption of 50 ml of E. billardieri hydrosol as a complementary treatment in diabetic patients reduced HbA1C and cholesterol levels without adverse effects on the liver or kidneys functions.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Antidiabetic activity, Blood lipid profile, Glycemic Index, Glycosylated hemoglobin, Medicinal plant</keyword>
				<start_page>34</start_page>
				<end_page>44</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21175.html</web_url>
			<author_list><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Hamami Chamgordani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hamami_z@yahoo.com</email>
				<code>91678</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Adult Health Nursing, Faculty of Nursing and Midwifery, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Mazaheri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mazaherimohammad@yahoo.com</email>
				<code>91679</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Medicine, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bijan</first_name>
				<middle_name></middle_name>
				<last_name>Iraj</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>bijaniraj@gmail.com</email>
				<code>91680</code>
				<coreauthor>No</coreauthor>
				<affiliation>Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hojjat</first_name>
				<middle_name></middle_name>
				<last_name>Baghshahi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>baghshahi_h1989@yahoo.com</email>
				<code>91681</code>
				<coreauthor>No</coreauthor>
				<affiliation>Barij Medicinal Plants Research Center, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fakhri</first_name>
				<middle_name></middle_name>
				<last_name>Sabouhi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sabohi@nm.mui.ac.ir</email>
				<code>91682</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Adult Health Nursing, Faculty of Nursing and Midwifery, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>The effects of phytosomal curcumin supplementation on clinical symptoms, and inflammatory and oxidative stress biomarkers in patients with migraine: A protocol for a randomized double-blind placebo-controlled trial</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Migraine is one of the most common diseases. Curcumin with anti-oxidative and anti-neuroinflammatory properties might have beneficial effects in migraine patients. This study will be conducted to evaluate the effects of a phytosomal preparation of curcumin on clinical signs, oxidative stress, and inflammatory parameters in patients with migraine.Materials and Methods: This is a randomized, double-blind, placebo-controlled, clinical trial in which, 60 patients with migraine will be assigned to receive a daily dose of 250 mg of phytosomal curcumin for 8 weeks (intervention group) or 250 mg maltodextrin as a placebo for the same duration (control group). Before and after the study, frequency, duration, and severity of the attacks, quality of life and sleep, mood status, high-sensitivity C-reactive protein (hs-CRP), Nitric Oxide (NO), and oxidative stress factors will be measured.Conclusion: It seems that phytosomal formulation of curcumin (a solid dispersion preparation of curcumin with phosphatidylserine) with high bioavailability, can cross the blood-brain barrier (BBB) and result in decreased neuroinflammation, oxidative stress, and neurotoxicity. This way, phytosomal curcumin might lead to reduction of headaches and other complications of migraine and increase the quality of life of patients with migraine. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Curcumin, Phytosomal curcumin, Migraine, Inflammation, Headache</keyword>
				<start_page>45</start_page>
				<end_page>57</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21242.html</web_url>
			<author_list><author>
				<first_name>Mehrnaz</first_name>
				<middle_name></middle_name>
				<last_name>Shojaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mehrnaz.shojaei97@yahoo.com</email>
				<code>92049</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Amirhossein</first_name>
				<middle_name></middle_name>
				<last_name>Sahebkar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sahebkara@mums.ac.ir</email>
				<code>92050</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fariborz</first_name>
				<middle_name></middle_name>
				<last_name>Khorvash</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fkhorvash@gmail.com</email>
				<code>92051</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Soheil</first_name>
				<middle_name></middle_name>
				<last_name>Fallahpour</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>dr.sfallahpour@gmail.com</email>
				<code>92052</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gholamreza</first_name>
				<middle_name></middle_name>
				<last_name>Askari</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>askari@mui.ac.ir</email>
				<code>92053</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nutrition and Food Security Research Center and Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Anesthesia and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Bagherniya</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>bagherniya@nutr.mui.ac.ir</email>
				<code>92054</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Nutrition and Food Security Research Center and Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Anesthesia and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>The effect of hydroalcoholic extract of Cichorium intybus leaf on aryl hydrocarbon receptor expression in the testis of Wistar rats exposed to cigarette smoke</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Cigarette smoke (CS) contains compounds such as reactive oxygen species (ROS). Oxidative stress caused by excessive ROS eventually leads to germ cell apoptosis and male infertility. The leaves of Cichorium intybus (chicory) are rich in natural antioxidants, but their protective effects on the adverse effects of CS on testicular tissue have not been studied.Materials and Methods: 24 Wistar rats were classified into four groups: control, extract: treatment with chicory extract (200 mg/kg body weight/day) for 13 weeks, smoke: exposed to CS for 13 weeks, and smoke + extract: exposed to CS and treated with the C. intybus extract. Histological and biochemical analyses and apoptosis assay were done, and Ahr, and Cyp1a1 expression was determined.Results: Treatment with C. intybus compensated for the reduction of Sertoli cells, spermatogonia, spermatocytes, and spermatids caused by CS. Chicory extract reduced free radicals and improved antioxidant status. The lowest and highest percentage of apoptotic cells was observed in the extract and smoke groups, respectively, while simultaneous treatment with C. intybus extract led to a significant reduction of apoptotic cells. The mean Ahr levels in the control, extract, smoke and smoke + extract groups were 1.00±0.57, 1.93±0.25, 5.98±0.42, and 0.62±0.22, respectively (p˂0.05). The mean levels of Cyp1a1 expression in the control, extract, smoke and smoke + extract groups were 1.00±0.31, 2.28±0.65, 5.55±0.40, and 0.21±0.23 (p˂0.05).Conclusion: The C. intybus extract probably affected Cyp1a1 expression by downregulation of Ahr. These led to a decrease in free radicals and apoptosis, and an improvement in antioxidant status.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cichorium Intybus, Spermatogenesis, Malondialdehyde, Caspase-3, Cigarette smoke</keyword>
				<start_page>58</start_page>
				<end_page>69</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21307.html</web_url>
			<author_list><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Hashemi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mh12311@gmail.com</email>
				<code>92398</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahnaz</first_name>
				<middle_name></middle_name>
				<last_name>Azarnia</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>azarnia@khu.ac.ir</email>
				<code>92399</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Hajebrahimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hajebrahimi@ari.ac.ir</email>
				<code>92400</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>A&amp;S Research Institute, Ministry of Science Research and Technology, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Samad</first_name>
				<middle_name></middle_name>
				<last_name>Nejad Ebrahimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>s_ebrahimi@sbu.ac.ir</email>
				<code>92401</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Phytochemistry, Medicinal Plants and Drugs Research Institute, Shahid Beheshti University, G. C., Evin, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>The effects of Artemisia absinthium L. on scopolamine-induced learning and memory impairment and brain tissue oxidative damage in adult rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: The present study examined the effects of Artemisia absinthium L. on scopolamine-induced memory dysfunction and brain tissue oxidative damage in rats. Materials and Methods: Fifty rats were used in five groups: Control: received dimethyl sulfoxide (DMSO)/saline, Scopolamine: scopolamine (2 mg/kg) was administered along with DMSO/saline, and Scopolamine-Ext 50, Scopolamine-Ext 100, and Scopolamine-Ext 200 groups: A. absinthium hydroalcoholic extract 50, 100 and 200 mg/kg were administered before scopolamine. The Morris water maze (MWM) and passive avoidance (PA) tasks were used for assessment of behavioral parameters. Malondialdehyde (MDA), nitric oxide (NO) metabolites, total thiol, catalase (CAT), and superoxide dismutase (SOD) were measured in the cortex and hippocampus.Results: A. absinthium decreased the delay time and distance traveled to reach the platform in the MWM test (p&lt;0.05-p&lt;0.001). Besides, the extract increased the delay time to pass in the dark and the light time while decreasing the number of entrances and the dark time in the PA task (p&lt;0.05-p&lt;0.001). In biochemical assessments, A. absinthium attenuated NO metabolites (p&lt;0.001) and MDA (p&lt;0.05- p&lt;0.001) while enhanced total thiol (p&lt;0.001), CAT and SOD (both p&lt;0.05-p&lt;0.001).Conclusion: This study revealed that A. absinthium improved memory and learning impairment and brain tissue oxidative damage in scopolamine-treated rats. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Artemisia absinthium, Memory, Oxidative stress, Scopolamine</keyword>
				<start_page>70</start_page>
				<end_page>84</end_page>
				<web_url>https://ajp.mums.ac.ir/article_20758.html</web_url>
			<author_list><author>
				<first_name>Marzieh</first_name>
				<middle_name></middle_name>
				<last_name>Rahimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rahimimr98@gmail.com</email>
				<code>89772</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Narges</first_name>
				<middle_name></middle_name>
				<last_name>Marefati</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>narges.marefati206@gmail.com</email>
				<code>89773</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology and Medical Physics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Farimah</first_name>
				<middle_name></middle_name>
				<last_name>Beheshti</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>beheshtif1@thums.ac.ir</email>
				<code>89774</code>
				<coreauthor>No</coreauthor>
				<affiliation>Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Somaieh</first_name>
				<middle_name></middle_name>
				<last_name>Ahmadabady</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ahmadabadis971@mums.ac.ir</email>
				<code>89775</code>
				<coreauthor>No</coreauthor>
				<affiliation>Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hassan</first_name>
				<middle_name></middle_name>
				<last_name>Rakhshandeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rakhshandehh@mums.ac.ir</email>
				<code>89776</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahmoud</first_name>
				<middle_name></middle_name>
				<last_name>Hosseini</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hosseinim@mums.ac.ir</email>
				<code>89777</code>
				<coreauthor>No</coreauthor>
				<affiliation>Psychiatry and Behavioral Sciences Research Center, Mashhad Universityof Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>The hematopoietic potential of methanolic and aqueous extracts of Portulaca oleracea in a phenylhydrazine model of anemia</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Portulaca oleracea, commonly known as Purslane, is traditionally used as a sour, diuretic, and cooling herb with hemostatic properties. The present study evaluates the antianemic effect of methanolic and aqueous extracts of P. oleracea in a phenylhydrazine model of anemia.Materials and Methods: Phenylhydrazine (60 mg/kg/day, i.p., two consecutive days) was used to induce anemia in rats. The aqueous and methanolic extracts of P. oleracea were prepared, and three methods of treatment were defined with two doses (500 and 750 mg/kg, i.p.). The hematological parameters and blood cell morphology, total and direct bilirubin, and morphology, and pathology of bone marrow were evaluated.Results: The results showed that the methanolic extract has better effects than aqueous extract in improving phenylhydrazine-induced anemia. Our results showed that administration of 500 and 750 mg/kg of P. oleracea methanolic extracts for 4 days could protect against the development of anemia caused by phenylhydrazine.Conclusion: In summary, the methanolic extracts of P. oleracea might be effective in phenylhydrazine-induced anemia.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Purslane, Phenylhydrazine, Anemia, Methanolic extract, Aqueous extract</keyword>
				<start_page>85</start_page>
				<end_page>96</end_page>
				<web_url>https://ajp.mums.ac.ir/article_20965.html</web_url>
			<author_list><author>
				<first_name>Kobra</first_name>
				<middle_name></middle_name>
				<last_name>Shirani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>k.shirani@modares.ac.ir</email>
				<code>90717</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bamdad</first_name>
				<middle_name></middle_name>
				<last_name>Riahi-Zanjani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>riahib@mums.ac.ir</email>
				<code>90718</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Navid</first_name>
				<middle_name></middle_name>
				<last_name>Omidkhoda</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>omidkhodan991@mums.ac.ir</email>
				<code>90719</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Samira</first_name>
				<middle_name></middle_name>
				<last_name>Barangi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>barangis4001@mums.ac.ir</email>
				<code>90720</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gholamreza</first_name>
				<middle_name></middle_name>
				<last_name>Karimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>karimig@mums.ac.ir</email>
				<code>90721</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
Pharmaceutical Research Center, Institute of Pharmaceutical Technology, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>The protective effect of curcumin on thrombin-induced hyper-permeability</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Research Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective: Thrombin is a proinflammatory and pro-coagulant agent which is upregulated in several human diseases. Thrombin has a critical role in promoting cell proliferation and microvascular leakage in malignant cells, resulting in cancer growth and progression. Here, we explored the potential therapeutic value of curcumin on permeability induced by thrombin in mice.Materials and Methods: To assess the activity of curcumin on thrombin-induced vascular permeability mice model, C57BL / 6 mice were randomly divided into four groups: (1) control (2) Thrombin (3) Thrombin + Curcumin and (4) Thrombin + Metformin. Thirty minutes after treatment, Evans blue was injected intravenously through the tail vein to mice. Then, animals were sacrificed and the dye was extracted from the skin tissue by incubation with formamide. Heatmap and correlation map were generated and protein-protein interaction network of the hub genes was drawn by Cytoscape software.Results: Hub DEG expression rate showed that Heat shock protein a1 (Hspa1) family (comprised of HSPa1a, b, and HSPa5), caspase 3, and minichromosome maintenance complex component 2 were overexpressed after treatment with curcumin. Functional modules of curcumin enriched through Enrich gene biological process and revealed positive association of gene expression of apoptosis process with the therapy. Curcumin was also found to reduce leucocyte migration in murine tissues. Additionally, treatment with curcumin resulted in downregulation of heat shock proteins and proinflammatory cytokines such as monocyte chemotactic protein 1, interleukin-6 and chemokine (C-X-C motif) ligand 3.Conclusion: Curcumin inhibited the proinflammatory cytokines and inflammatory HSPs in endothelial cells and reduced thrombin-induced barrier destabilization in vivo.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Thrombin, Curcumin, Vascular permeability</keyword>
				<start_page>97</start_page>
				<end_page>108</end_page>
				<web_url>https://ajp.mums.ac.ir/article_21025.html</web_url>
			<author_list><author>
				<first_name>Farzad</first_name>
				<middle_name></middle_name>
				<last_name>Rahmani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rahmany.farzad@gmail.com</email>
				<code>90943</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Abdeahad</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>abdeahadh951@mums.ac.ir</email>
				<code>90944</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Najmeh</first_name>
				<middle_name></middle_name>
				<last_name>Jaberi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>jaberin2@mums.ac.ir</email>
				<code>90945</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Reyhane</first_name>
				<middle_name></middle_name>
				<last_name>Hanaie</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hanaier@mums.ac.ir</email>
				<code>90947</code>
				<coreauthor>No</coreauthor>
				<affiliation>Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Atena</first_name>
				<middle_name></middle_name>
				<last_name>Soleimani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>soleimaniat961@mums.ac.ir</email>
				<code>90946</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Amir</first_name>
				<middle_name></middle_name>
				<last_name>Avan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>avana@mums.ac.ir</email>
				<code>90949</code>
				<coreauthor>No</coreauthor>
				<affiliation>Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Majid</first_name>
				<middle_name></middle_name>
				<last_name>Khazaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>khazaeim@mums.ac.ir</email>
				<code>90950</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Mahdi</first_name>
				<middle_name></middle_name>
				<last_name>Hassanian Mehr</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hasanianmehrm@mums.ac.ir</email>
				<code>90951</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>