Berberine Attenuated Oxidative Stress Induced by Sodium Nitrite in Rat Liver

Berberine is a well-known alkaloid derived from Berberis species. The present study aimed to investigate the hepatoprotective properties of berberine and elucidate its probable mechanisms against sodium nitrite toxicity. 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. Treatment of rats with sodium nitrite considerably increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, malondialdehyde (MDA) content, tumor necrosis factor (TNF)-α expression, caspase-3 activity, and transforming growth factor (TGF)-β1 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. 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.