Taraxerol Acetate: A Natural Hepatoprotective Agent against Drug-Induced Liver Damage.
DOI:
https://doi.org/10.64105/s5rdpf04Keywords:
Taraxerol acetate, CCl₄-Induced Hepatotoxicity, Hepatoprotective AgentsAbstract
Background: Drug-induced liver injury is a significant clinical concern, often resulting in acute or chronic liver dysfunction. Carbon tetrachloride (CCl₄) serves as a widely used experimental model to induce hepatotoxicity and evaluate the protective efficacy of therapeutic agents. Taraxerol acetate (TA), a natural compound with promising antioxidant and anti-inflammatory properties, has demonstrated hepatoprotective potential in preclinical studies. This study investigates the hepatoprotective effects of TA against CCl₄-induced liver damage in Wistar albino rats.
Methods: A total of 25 adult Wistar albino rats were divided into five groups: normal control, negative control (CCl₄-only), positive control (silymarin-treated), and two test groups receiving TA at doses of 20 mg/kg and 40 mg/kg. Treatments were administered orally or intraperitoneally for three days, with subcutaneous CCl₄ administration on the third day to induce hepatotoxicity. Blood samples were collected post-treatment to measure biochemical markers of liver injury, including serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (ALP), and total bilirubin (TB). Statistical analysis was performed using ANOVA with a significance threshold of p < 0.05.
Results: CCl₄ exposure significantly elevated liver enzyme levels and reduced liver weight in the negative control group. TA treatment at 20 mg/kg and 40 mg/kg doses markedly decreased SGOT, SGPT, ALP, and TB levels (p < 0.05) and improved liver weight compared to the negative control. The hepatoprotective effect of TA was comparable to the standard drug silymarin. Notably, the 20 mg/kg dose exhibited the most pronounced reduction in liver enzyme levels.
Conclusion: Taraxerol acetate demonstrated significant hepatoprotective effects against CCl₄-induced liver damage, with reductions in biochemical markers of liver injury and improved liver weight. These findings suggest that TA is a promising candidate for the prevention and management of drug-induced liver injury. Further clinical investigations are warranted to confirm its therapeutic potential in humans.




