It displays a wide variety of pharmacological properties, including antioxidant, anti-carcinogenic and anti-inflammatory effects. This study was done to explore the role of fisetin, in ameliorating oxidative damage in thioacetamide (TAA)-induced hepatic injury in rats. Thirty-six male albino rats were divided into three equal groups. Group I (normal control group): rats administered distilled water only. Group II (TAA-intoxicated group): rats received thioacetamide (50 mg/kg b. wt.) intraperitoneally twice weekly for 6 weeks. Group III (TAA + fisetin co-treated group): rats received thioacetamide (50 mg/kg b. wt.) and at the same time administered fisetin (10mg/ kg b. wt. /daily /orally) for 6 weeks (end of experiment). All animals were sacrificed after 6 weeks. The results revealed that serum levels of Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP) were significantly elevated in Group II. Oxidative stress in the group II was manifested by a significant rise in Malondialdehyde (L-MDA) levels with a marked reduction in Glutathione (GSH) content and diminished activity of antioxidant enzyme Glutathione-S-Transferase (GST), in liver tissues as compared with the control group. The coadministration of fisetin and thioacetamide (protection modality) restored the thioacetamide induced alterations in liver functions, promoted oxidative stress and antioxidant defense. Thus, the results of the present study indicate that fisetin treatment protects the hepatocytes by improving the antioxidant competence in hepatic tissues of thioacetamide intoxicated rats.

Curcumin [1,7-bis (4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] was shown to exert potent antioxidant, anti-inflammatory and hepatoprotective properties. This study was done to investigate the protective effects of curcumin in thioacetamide (TAA)-induced hepatic injury in rats. Thirty-six male albino rats were divided into three equal groups. Group I (normal control group). Group II (TAA-intoxicated group): rats received thioacetamide (50 mg/kg b. wt. ip) twice weekly for 6 weeks. Group III (TAA + curcumin co-treated group): rats received thioacetamide (50 mg/kg b. wt.) and simultaneously administered curcumin (200 mg/kg b. wt./daily/orally) for 6 weeks (end of experiment). All animals were sacrificed after 6 weeks. TAA administration induced liver damage manifested by the significant increases in serum levels of ALT, AST, ALP and total bilirubin compared with control group. Oxidative stress in the group II was manifested by a significant rise in L-MDA levels with a marked reduction in the activities of antioxidant enzymes like GST, catalase CAT and depletion of GSH content in liver tissues as compared with the control group. On the other hand, TAA significantly affected the inflammation markers represented by elevation of myeloperoxidase (MPO) activities and upregulation of interleukin-6 (IL-6) gene expression levels in liver tissues. The coadministration of curcumin and thioacetamide (protection modality) prevented liver injury by normalizing the biochemical parameters, lipid peroxidation index and improving the protein oxidation, inflammatory markers and the antioxidant status. These findings suggested that, liver injury could be curtailed by the antioxidant and anti-inflammatory activities of curcumin and the normal status of the liver could be preserved.