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Year : 2019  |  Volume : 47  |  Issue : 2  |  Page : 80-86

Effects of berberine on high-fat/high-sucrose-induced nonalcoholic steatohepatitis in experimental rats

Medical Biochemistry Department, Tanta University, Tanta, Egypt

Correspondence Address:
Elrefaei Eman
BSc of Medicine and Surgery Faculty of Medicine, Tanta University, Elgarbia, 3151
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DOI: 10.4103/tmj.tmj_15_18

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Background Nonalcoholic steatohepatitis (NASH) is the most common chronic liver disease in the world, characterized by hepatic steatosis, inflammation, hepatocyte injury with or without fibrogenesis, which might lead to cirrhosis. Berberine (BBR) is a natural isoquinoline alkaloid with very impressive health benefits. Aim The aim of the study is to evaluate the protective effect of BBR in experimental NASH induced by high-fat/high-sucrose diet in male albino rats. Materials and methods Sixty male albino rats were divided randomly into four equal groups: group I (normal control group), group II (BBR-treated control group), group III (NASH group), and group IV (BBR-treated NASH group). Levels of peroxisome proliferator gamma receptor coactivator one alpha (PGC-1α) in hepatic nuclear extract were measured by enzyme-linked immunosorbent assay, while the activity of cytosolic glycerol-3-phosphate dehydrogenase 1 in the liver tissue homogenate, liver enzymes, lipid profile, and plasma ferric reducing/antioxidant power were measured spectrophotometrically. Results There was a statistically significant decrease of hepatic PGC-1α, plasma ferric reducing/antioxidant power, serum high-density lipoprotein-cholesterol along with a significant increase in the activity of glycerol-3-phosphate dehydrogenase 1, liver enzymes as well as hyperlipidemia in the NASH group were compared with both normal control and BBR-treated control groups. These pathological disturbances were significantly ameliorated by BBR supplementation. Conclusion The present study provided unequivocal evidence that disturbed hepatic PGC-1α and altered redox status acted as major contributing factors for the pathogenesis of high-fat/high-sucrose-induced NASH in rats. It also shed some light on the potential therapeutic value of BBR in NASH, partly accredited to its hypolipidemic and antioxidant effects, in addition to upregulating the levels of PGC-1α in hepatic nuclear extracts.

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