Introduction: Paracetamol, a commonly used antipyretic and analgesic, can induce liver damage due to oxidative stress, particularly with prolonged use or overdoses. This study assessed the hepatoprotective effects of Corchorus depressus against paracetamol-induced toxicity in HepG2 cells and Wistar albino rats. Methods: Sequential extracts of C. depressus were analyzed for antioxidant activity using DPPH, ABTS, NO, and H2O2 scavenging assays, reducing power, and β-carotene bleaching methods. Among these, the ethyl acetate extract (CDEAE) exhibited the highest antioxidant activity. In HepG2 cells, CDEAE enhanced cell viability and normalized toxicity markers, including AST, ALT, LDH, lipid peroxidation, and GSH levels. Results: In vivo studies revealed that paracetamol administration caused severe liver damage, indicated by elevated hepatic markers (AST, ALT, ALP, TBIL), decreased total protein (TP), increased oxidative stress (MDA), and reduced antioxidant enzymes (SOD, CAT, GSH). Cotreatment with CDEAE significantly improved these parameters. Histopathological analysis confirmed reduced liver necrosis and inflammation. Conclusion: These findings demonstrate that C. depressus, particularly its ethyl acetate extract, offers significant hepatoprotective effects attributed to its potent antioxidant properties, suggesting its potential as a therapeutic agent for paracetamol- induced liver injury. conclusion: These findings demonstrate that C. depressus, particularly its ethyl acetate extract, offers significant hepatoprotective effects attributed to its potent antioxidant properties, suggesting its potential as a therapeutic agent for paracetamol-induced liver injury.
Pareek et al. (Tue,) studied this question.