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Background and aim Liver cirrhosis is a global syndrome that develops from activation and proliferation of hepatic stellate cells, and following extracellular matrix accumulation. The current study evaluates the acute toxicity and prophylactic effects of mangiferin in thioacetamide (TAA)-induced liver damage in rats and its causal mechanisms. Experimental procedure Thirty Sprague–Dawley rats were separate into five groups and treated for two months as follows: group (A) normal ingested orally daily 10% Tween 20 + distilled water (i.p.) (three times weekly); group (B) TAA control rats treated by mouth daily 10% Tween 20 + 200 mg/kg TAA i.p. (three times weekly); group (C) reference group received daily oral dose of 50 mg/kg silymarin + 200 mg/kg TAA i.p. (three times weekly); groups (D) rats received oral daily 30 mg/kg mangiferin + 200 mg/kg TAA i.p. (three times weekly); group (E) received oral daily 60 mg/kg mangiferin + 200 mg/kg TAA i.p. (three times weekly) for two months. Results The non-toxic effects of mangiferin were evidenced by the lack of any toxicity incidence in rats ingested with up to 500 mg/kg. Gross morphological examination showed a regular liver architecture in mangiferin fed collections compared to hepatotoxic cluster. Histology of rat’s liver fed with mangiferin showed an important decrease in the liver index with hepatic cells propagation, mild cellular injury. Macroscopy of hepatotoxic liver exhibited irregular, rough surface with micro and macro nodules, and histopathology-stained Hematoxylin and Eosin (H&E), and Masson’s Trichome exhibited inflammation infiltration of lymphocytes, focal necrosis, fibrosis, and bile duct propagation. Immunohistochemistry examination of proliferation cellular nucleus antigen (PCNA), TAA inoculation stimulated cellular proliferation and apoptotic actions in damaged liver tissues, designated by increased PCNA. The TAA intraperitoneal inoculation caused significant hepatic dysfunction (lowered total protein, albumin levels, hepatotoxicity, and necrotic cell propagation). The TAA injection aggravated important hepatic intoxication inveterate by histopathological symptoms; change of tissue architecture, cellular propagation, and endothelial harm, enlarged hepatic nucleus, cytoplasmic vacuolation, collagen deposition, and raised necrotic tissues. The oxidative stress and inflammation process was markedly commenced subsequent TAA conveyance to rats proved by down-regulation of SOD, CAT, and IL-10, while, up-regulating the MDA and TNF-α and IL-6 cytokines. Conclusion No toxicological signs were observed in rats administered 500 mg/kg of Mangiferin. Mangiferin supplementation showed significant resistance against TAA-mediated hepatotoxicity, reversed those cellular alterations, and restored liver functions. These results demonstrate significant ameliorative effects of mangiferin in TAA hepatotoxic rats, which could be attributed to its anti-apoptotic, antioxidant, and anti-inflammatory potentials, making it a possible viable hepatoprotective agent for inflammatory-related hepatitis.