Berberine mitigates acetamiprid-induced hepatotoxicity and inflammation via regulating endogenous antioxidants and NF-κB/TNF-α signaling in rats.

Acetamiprid is a neonicotinoid insecticide used on a large scale and has been reported for oxidative stress-mediated toxicity and physiological alterations in mammals. The plant-derived natural antioxidant berberine (BBR) possesses protective potential against inflammation, structural changes, and cellular toxicity. The current study aimed to investigate the toxic effects of acetamiprid exposure and the antioxidative and anti-inflammatory efficacy of BBR in rat liver tissue. The results showed that intragastric exposure of acetamiprid (21.7 mg/kg b.wt, i.e., 1/10 of LD50) for 21 days significantly elicited oxidative stress as evidenced by lipid peroxidation, protein oxidation, and depletion of endogenous antioxidants. Furthermore, acetamiprid exposure elevated NF-κB, TNF-α, IL-1β, IL-6, and IL-12 expression and caused structural alterations in liver tissue. Biochemical results showed that 2-h pre-treatment of BBR (150 mg/kg b.wt; 21 days) reduced damage to lipids and proteins, replenished GSH, enhanced SOD and catalase activities, and offered antioxidative effects against acetamiprid toxicity. Also, BBR suppressed inflammation by regulating NF-κB/TNF-α signaling in hepatic tissue of acetamiprid-intoxicated rats. Histopathological examination confirmed the hepatoprotective effects of BBR. Our findings indicate that BBR might be a potential ameliorative agent against oxidative stress-mediated hepatotoxicity.