Methanolic Extract Ameliorates CCl-Induced Liver Injury by Modulating Oxidative Stress, Inflammatory, and Apoptotic Markers in Rats.

The main objective of this study was to investigate the hepatoprotective potency of the methanol extract against CCl-induced liver damage in rats. HPLC technique was used to estimate the presence of polyphenols in the methanol extract of (PCM), while proximate analysis revealed the presence of carbohydrates, lipids, and moisture in the extract. The antioxidant potential of PCM was evaluated by 2,2-diphenylpicrylhydrazyl (DPPH) and reducing power assay, which showed a high percentage of inhibition against free radicals. Hepatotoxicity was induced by carbon tetrachloride (CCl). CCl administration reduced the activity of endogenous antioxidants, whereas it increased the production of nitrites and hydrogen peroxide (HO) in rats. Furthermore, the level of hepatic markers in serum was also elevated after CCl administration. Moreover, the expression of stress-related markers, proinflammatory mediators, and apoptotic genes was enhanced in CCl-treated rats. Coadministration of PCM along with CCl in rats reduced the levels of free radicals and the above genes to normal levels. CCl administration caused histopathological alterations in liver tissues, while cotreatment with PCM mitigated liver injuries. These findings suggest that the methanol extract of possesses antioxidant and anti-inflammatory properties and can prevent liver injury. Further pharmacological research will be helpful in determining the effectiveness of in humans. Development of FDA-approved plant-based anti-inflammatory drugs can help treat patients and reduce the chances of toxicity.