Abstract
Tea polyphenols (TPs), which are derived from tea extracts, are a class of chemicals containing polyphenol hydroxyls that have been observed to have strong anti-oxidative properties. Previous studies have demonstrated that TP can protect against hepatic ischemia/reperfusion (I/R) injury; however, the underlying mechanism remains unknown. In the present study, the mechanism underlying TPs protective effects against I/R-induced liver damage was investigated, focusing on its anti-oxidative and anti-apoptotic bioactivities. C57BL/6 mice were used to establish a hepatic I/R-induced injury model, and liver injury was analyzed using a biochemical assay. The results from the current study demonstrated that the serum expression levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly increased in mice following hepatic I/R injury, while the ratio of hepatic glutathione (GSH)/oxidized GSH (GSSG) was reduced, indicating that liver damage had occurred. In mice that were orally administered with TP (50 mg/kg) 1 h prior to I/R-induced injury, the extent of liver injury was significantly attenuated. It was also observed that I/R injury significantly decreased the mRNA and protein expression levels of cytokine-inducible nitric oxide synthase in liver tissues, and this was also attenuated by pretreatment with TP. Furthermore, pretreatment with TP significantly attenuated the I/R-induced increase in liver cell apoptosis, and the expression level and activity of pro-apoptotic proteins in the liver, indicating that I/R-induced liver cell apoptosis is inhibited by TP. In conclusion, the results in the present study suggest that TP protects against hepatic I/R-induced injury by inhibiting I/R-induced oxidative damage and liver cell apoptosis.