Hepatoprotective Effects and Ameliorative Potential of Solanum nigrum Leaf Extract on Biochemical and Histological Alterations in CCl4-Induced Liver Injury in Rats

Abstract

Hepatotoxicity, characterized by liver dysfunction or damage caused by excessive drug or xenobiotic exposure, remains a significant health concern. This study aimed to assess the hepatoprotective effects and ameliorative potential of the aqueous leaf extract of Solanum nigrum against carbon tetrachloride (CCl4)-induced liver toxicity in rats. Thirty male albino rats were divided into six groups (five rats each): a normal control group, a hepatotoxic control group receiving only CCl4, and four treatment groups. The hepatotoxic groups were administered a single dose of 1.5 ml/kg body weight of CCl4 intraperitoneally. Treatment groups received CCl4 alongside either 200 mg/kg silymarin (standard drug), or 50 mg/kg, 100 mg/kg, or 200 mg/kg of Solanum nigrum aqueous leaf extract orally for 14 days. Liver function markers and antioxidant parameters—including reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)—were evaluated. CCl4 administration significantly elevated liver enzyme levels and decreased antioxidant enzyme activities compared to control. However, treatment with Solanum nigrum extract significantly lowered liver enzymes and improved antioxidant status (P < 0.05) relative to the untreated hepatotoxic group. Histological analysis revealed that CCl4 caused severe liver damage, including disrupted cellular architecture, portal vein congestion, inflammatory infiltration, hemorrhage, and necrosis. Conversely, treatment with the extract restored normal liver histology. The extract restored liver function indices and antioxidant enzyme levels towards normal, comparable to the effect of silymarin, indicating that S. nigrum could serve as an effective natural hepatoprotective agent. These findings demonstrate that the aqueous leaf extract of Solanum nigrum effectively protects against CCl4-induced liver damage and mitigates its adverse effects in albino rats.