Tea polyphenols protect against ischemia/reperfusion-induced liver injury in mice through anti-oxidative and anti-apoptotic properties

Tao,Jin; Shen,Xinhong; Ai,Yonghong; Han,Xiaojing

doi:10.3892/etm.2016.3789

Tea polyphenols protect against ischemia/reperfusion-induced liver injury in mice through anti-oxidative and anti-apoptotic properties

Authors:
- Jin Tao
- Xinhong Shen
- Yonghong Ai
- Xiaojing Han
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Affiliations: Department of Nephrology, Xinxiang Central Hospital, Xinxiang, Henan 453000, P.R. China, Blood Purification Room, Xinxiang Central Hospital, Xinxiang, Henan 453000, P.R. China
Published online on: October 11, 2016 https://doi.org/10.3892/etm.2016.3789
Pages: 3433-3439

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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.

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