1Medicinal Plants Research Center, Yasuj University of Medical Sciences, Yasuj, Iran
2Student Research Committee, Yasuj University of Medical Sciences, Yasuj, Iran
3Social Determinants of Health Research Center, Yasuj University of Medical Sciences, Yasuj, Iran
4Cellular and Molecular Research Center,Yasuj University of Medical Sciences, Yasuj, Iran
5Department of Pharmacology, Faculty of Medicine, Yasuj University of Medical Sciences, Yasuj, Iran
Objective: The present study was conducted to investigate the hepatoprotective activity of hydro-ethanolic fruit extract of Rosa canina (R. canina) against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Methods: Male Wistar albino rats were randomly divided into six groups of 8 animals of each, including control, toxic (CCl4), R. canina 250, 500, and 750 mg/kg + CCl4 and R. canina 750 mg/kg alone. R. canina (p.o., daily) and CCl4 (1 ml/kg twice a week, 50% v/v in olive oil, i.p.) were administered to animals for six weeks. Serum analysis was performed to assay the levels of aspartate aminotransferase (AST), alanine amino transaminase (ALT), alkaline phosphatase (ALP), albumin (ALB), total protein (TP) and malondialdehyde (MDA). Biochemical observations were also supplemented with histopathological examination (haematoxylin and eosin staining) of liver section. Results: Hepatotoxicity was evidenced by considerable increase in serum levels of AST, ALT, ALP, and lipid peroxidation (MDA) and decrease in levels of ALB and TP. Injection of CCL4 also induced congestion in central vein, and lymphocyte inﬁltration. Treatment with hydro-alcoholic fruit extract of R. canina at doses of 500 and 750 mg/kg significantly reduced CCl4-elevated levels of ALT, AST, ALP and MDA (p<01). The extract also increased the serum levels of ALB and TP compared to CCl4 group (p<01) at the indicated dose Histopathological studies supported the biochemical finding. Conclusion: our finding indicated hepatoprotective effects of the hydro-alcoholic fruit extract of R. canina on CCl4-induced hepatic damage in rats and suggested that theses effect may be produced through reducing oxidative stress.
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