berberine attenuated oxidative stress induced by sodium nitrite in rat liver

Background: berberine is a well-known alkaloid derived from berberis species. objectives: the present study aimed to investigate the hepatoprotective properties of berberine and elucidate its probable mechanisms against sodium nitrite toxicity. methods: forty animals were randomly classified into five equal groups to be treated for 60 days, including group 1: control, group 2: berberine-treated (100 mg/kg), group 3: sodium nitrite-treated (80 mg/kg), group 4: sodium nitrite together with 50 mg/kg of berberine, and group 5: sodium nitrite together with 100 mg/kg of berberine. the protective effects of berberine against sodium nitrite induced-liver damage were investigated using parameters related to oxidative stress, inflammation, fibrosis, and apoptosis in the hepatocytes. results: treatment of rats with sodium nitrite considerably increased alanine aminotransferase (alt) and alkaline phosphatase (alp) activities, malondialdehyde (mda) content, tumor necrosis factor (tnf)- expression, caspase-3 activity, and transforming growth factor (tgf)- 1 concentration (p < 0.05) and significantly declined the levels of reduced glutathione (gsh), glutathione reductase (gr), glutathione s-transferase (gst), and glutathione peroxidase (gpx) (p < 0.05). the treatment of intoxicated rats with 100 mg/kg of berberine significantly reversed these changes and reached the values approximately to the normal level. however, berberine 50 mg/kg failed to normalize the disturbances. conclusions: this study demonstrated that berberine could decrease sodium nitrite-induced liver injury in a dose-dependent manner probably due to its antioxidant, anti-inflammatory, anti-apoptotic, and antifibrotic capacities.