Abstract

Berberine is a plant derived alkaloid present in many plants that may has ameliorating potential influences against inflammatory and oxidative conditions. The current study aimed to evaluate the possible protective activity of berberine and investigate its probable mechanisms against sodium nitrite toxicity in the liver. Forty male rats were divided into five groups. Group one, as the control group, received normal saline, group two received berberine (100 mg.kg-1), and group three received sodium nitrite (80 mg.kg-1). Groups four and five received berberine in doses of 50 and 100 mg.kg-1, respectively, and sodium nitrite (80 mg.kg-1) was given orally. All the doses were orally administrated for two months. Then, at the end of the 60th day, the animals were sacrificed, and the liver homogenate was prepared. For evaluating the oxidative injury the levels of albumin (ALB) and aspartate transaminase (AST) in the serum and oxidative stress parameters in the liver were analyzed. Treatment of rats with sodium nitrite considerably increased the levels of serum AST and liver superoxide anion and significantly reduced the levels of serum ALB, hepatic superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase (CAT) activity in the liver tissue. Berberine treatment could ameliorate all these parameters dose dependently. Berberine at a dose of 100 mg.kg-1 had the best impact and reached the values of oxidative stress parameters to the normal level. Our results demonstrated that berberine in a dose-dependent manner offered protection against sodium nitrite-induced oxidative injury in liver, which possibly reflects the antioxidant abilities of this alkaloid.

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