The Protective Effect of a Metallic Selenopeptide

Authors: Wang Cheng Shen Na Yan Ganglin Sui Chunhong Zhuang Jianjian Lü Shaowu Luo Guimin Mu Ying

Publish Date: 2014/02/15

Volume: 20, Issue: 3, Pages: 307-324

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Abstract

A 65mer peptide Se–CuZn–65P is an enzyme mimic with antioxidant activity of superoxide dismutase SOD and glutathione peroxidase GPX The metallic selenopeptide imitate was obtained through a single protein production system and cysteine auxotrophic expression technique and it enters cells in the assistance of the transactivator of transcription peptide Because Se–CuZn–65P was provided with the antioxidant activities of SOD and GPX it can be a potential drug for the prevention of alcoholic liver diseases Therefore the protective effects of Se–CuZn–65P on ethanolinduced L02 cells were evaluated in vitro Our results revealed that Se–CuZn–65P significantly protected the hepatocytes against ethanolinduced cell cytotoxicity which displayed by increase of cell viability migration and decrease of reactive oxygen species ROS malondialdehyde MDA lactate dehydrogenase LDH aspartate aminotransferase AST Furthermore the experiments of TUNEL assay flow cytometry assay expression levels determination of apoptosisrelated gene Bad Bax BclxL Bcl2 and protein procaspase3 PARP cleavage indicated that Se–CuZn–65P inhibited ethanolinduced L02 cell apoptosis Mechanically Se–CuZn–65P could attenuate the oxidative damage of mitochondria in ethanolinduced L02 cells Se–CuZn–65P prevented ethanoltriggered ROS and MDA generation in L02 cells and inhibited the release of the AST and LDH Se–CuZn–65P also restored the equilibrium of proapoptotic and antiapoptotic genes including Bad Bax BclxL and Bcl2 And the reduction of procaspase3 and the cleavages of PARP were attenuated by Se–CuZn–65P Thereby the L02 cell apoptosis were significantly prevented by treatment with Se–CuZn–65P mainly due to attenuation of oxidative stress In summary Se–CuZn–65P could prevent ethanolinduced liver injury through enhancing hepatocyte antioxidant abilities in intracellularThis research was supported by the National Natural Science Foundation of China No 31170740 and 31070772 Science and Technology Programs of Suzhou ZXG0920 Science and Technology Programs of Jinlin Province Educational Committee during the Twelfth Fiveyear Plan Period 2013–354

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