Hepatoprotective Effect of Aqueous Extract of Persian Gulf Brown Algae Sargassum swartzii Against Acetaminophen-Induced Hepatotoxicity in Mice

background: the liver plays an important role in detoxification of harmful materials and chemical agents. many medicines, such as acetaminophen, are potential for oxidative stress and liver toxicity. the brown algae sargassum swartzii possesses many pharmacological benefits. the present study investigated the aqueous extract of persian gulf brown algae sargassum swartzii effect on acetaminophen-induced liver injury in mice. objectives: it seems that persian gulf algae (sargassum swartzii) with its anti-inflammatory and antioxidant properties has preventive effects on acetaminophen-induced liver toxicity, yet no research has been reported in this regard so far. therefore, this study aimed at evaluating the effect of acetaminophen-induced liver toxicity in mice. methods: brown algae (sargassum swartzii) was collected from the low tide area of boushehr coasts, persian gulf). after transfer to the laboratory, the collected sample was washed with distilled water, air dried, and pulverized to powder. the air dried s. swartzii powder was soaked in 95% ethanol to remove pigments and small lipophilic molecules. the residue was then extracted with 10 ml of distilled water at 90°c for three hours, three times. all water extracts were combined, filtrated, and concentrated by water bath at 90°c and stored at 0°c for further analysis. hepatoprotective activity of the s. swartzii extract was confirmed by aspartate aminotransferase (ast), alanine aminotransferase (alt), and alkaline phosphatase (alp) levels and histopathologic findings as evidences. results: aqueous extract of s. swartzii at dose of 200 mg/kg showed a significant (p < 0.05) decrease in the levels of alt, ast, and alp, yet at dose of 100 mg/kg, it showed a significant (p < 0.05) decrease in the level of alt. conclusions: administration of the aqueous extract of s. swartzii (100 and 200 mg/kg) could improve hepatotoxicity induced by acetaminophen via change in liver marker enzymes and also improved histopathological alterations in liver tissue.