Dexamethasone-induced hepatic biochemical and pathological damages are attenuated by Cynodon dactylon extract containing hexadecanoic acid via reduction of glucose uptake: In vitro and in vivo studies

Mottaghian, Sadaf; Khalilarya, Ayshin; Malekinejad, Hassan

doi:10.22038/ajp.2025.26623

Dexamethasone-induced hepatic biochemical and pathological damages are attenuated by Cynodon dactylon extract containing hexadecanoic acid via reduction of glucose uptake: In vitro and in vivo studies

Articles in Press

Document Type : Original Research Article

Authors

¹ Department of Pharmacology and Toxicology, School of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran

² Experimental & Applied Pharmaceutical Sciences Research Center, Urmia University of Medical Sciences, Urmia, Iran

³ a Experimental & Applied Pharmaceutical Sciences Research Center, Urmia University of Medical Sciences, Urmia, Iran; b Department of Pharmacology and Toxicology, School of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran

10.22038/ajp.2025.26623

Abstract

Objective: The protective effects of ethanolic extract of Cynodon dactylon (CD) on dexamethasone (DEX)-induced hepatic injuries were investigated.
Materials and Methods: Following GC-MS phytochemical analyses of the extract, in vivo studies were conducted in male rats which were grouped as: control, dexamethasone (8mg/kg, intraperitoneally), DEX+CD (100, 200 and 400 mg/kg, orally), CD 400 and DEX+metformin (MET, 300mg/kg, orally) for 15 days. The in vitro studies were performed in HepG2 cells that grouped as: Control, DEX (1 µM), DEX+CD (0.1, 0.5 and 1 mg/ml), CD 0.5 mg/ml, and DEX+MET (500 µM). Cell viability and animal weight changes were recorded. Following the study period, biochemical and histopathological analyses were conducted on hepatic tissue and HepG2 cells.
Results: Findings revealed that CD extract does have concentration-dependent free radical-scavenging activity, and it possesses phenols and flavonoids contents. The most abundant compound of the CD extract was n-hexadecanoic acid. The DEX-induced hepatic functional enzymes and lactate dehydrogenase levels were significantly (p<0.05) reduced in both models. Moreover, the DEX-induced oxidative stress was improved by CD extract (45%). The DEX-elevated blood glucose (20%) and triglycerides (60%) were reduced in CD-treated animals. The DEX-generated hepatic macrovesicles and lipid droplets in HepG2 cells were reduced.
Conclusion: These results suggest that CD extract could be an effective compound for protection from DEX-induced hepatic injuries.

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