Protective Effect of Gallic Acid Against Thioacetamide Induced Metabolic Dysfunction of Lipids and Hepatic and Renal Toxicity
Abstract BackgroundGallic acid (GA) has a potential antioxidant bio-activity and inhibits diet-induced hypertriglyceridemia with reducing the size of adipocytes. GA also was found to increase the uptake of glucose by cell.MethodsThe present research studied the influence of gallic acid (GA) (100mg, 200 mg/Kg orally) on the liver and kidney injuries motivated by thioacetamide (TAA; 100 mg/Kg IP). The treatment of TAA was carried out three times weekly for eight weeks, while gallic acid was given daily. ResultsGA relieved the decrease of hepatic or renal reduced glutathione (GSH) or increase of malondialdehyde (MDA, an indicator for lipid peroxidation) induced by TAA. TAA treatment led to a significant increase in plasma inflammatory markers (TNF-α, CRP), liver enzymes (Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP) and kidney function parameters (creatinine, urea, uric acid). However, these parameters were reduced after treatment with GA. Moreover, GA reduced the significant decline in plasma protein induced by TAA. In addition, the hepatic fibrosis or histopathological changes of the liver and kidney were lowered by GA. ConclusionOur results suggested that GA may attenuate TAA induced liver and kidney toxicity via suppression of oxidative stress.