详细信息

Protective effect of resveratrol on rat cardiomyocyte H9C2 cells injured by hypoxia/reoxygenation by regulating mitochondrial autophagy via PTEN-induced putative kinase protein 1/Parkinson disease protein 2 signaling pathway  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Protective effect of resveratrol on rat cardiomyocyte H9C2 cells injured by hypoxia/reoxygenation by regulating mitochondrial autophagy via PTEN-induced putative kinase protein 1/Parkinson disease protein 2 signaling pathway

作者:Zhao Lixia[1,2,3];Sun Wei[4];Bai Decheng[1]

第一作者:赵丽霞;Zhao Lixia

通信作者:Bai, DC[1]

机构:[1]Lanzhou Univ, Sch Basic Med Sci, Inst Integrated Tradit Chinese & Western Med, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Sch Nursing, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Key Lab Dunhuang Med, Minist Educ, Lanzhou 730000, Peoples R China;[4]Lanzhou Univ, Hosp 1, Cardiac Surg, Lanzhou 730000, Gansu, Peoples R China

第一机构:Lanzhou Univ, Sch Basic Med Sci, Inst Integrated Tradit Chinese & Western Med, Lanzhou 730000, Peoples R China

通信机构:[1]corresponding author), Lanzhou Univ, Lanzhou 730000, Gansu, Peoples R China.

年份:2022

卷号:42

期号:2

起止页码:176

外文期刊名:JOURNAL OF TRADITIONAL CHINESE MEDICINE

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000792400200001)】;

基金:Supported by the Open Fund of Key Laboratory of Dunhuang Medicine, Ministry of Education (DHYX20-09) and the Youth Research Foundation of the Gansu University of Chinese Medicine (No. ZQ2017-14)

语种:英文

外文关键词:resveratrol; myocytes; cardiac; hypoxia; PTEN phosphohydrolase; Parkinson disease associated proteins; mitochondrial autophagy

摘要:OBJECTIVE: To investigate the protective effect of resveratrol on cardiomyocytes after hypoxia/reoxygenation intervention based on PTEN-induced putative kinase protein 1/Parkinson disease protein 2 (PINK1/PARKIN) signaling pathway. METHODS: 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to detect the effect of resveratrol on the viability of H9C2 cells; the hypoxia/reoxygenation (H/R) model was established in tri-gas incubator; 2', 7'-Dichlorofluorescin diacetate staining was used to measure the content of reactive oxygen species (ROS); the changes of mitochondrial membrane potential was determined by 5,5',6,6'-Tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide staining; the changes of mitochondrial respiratory chain complex activity was evaluated by enzyme activity kits; flow cytometry was used to detect the ratio of apoptotic cells; transmission electron microscope was used to observe the ultrastructure of H9C2 cells; Western blot was used to detect the protein changes of mitochondrial 20 kDa outer membrane protein (TOM20), translocase of inner mitochondrial membrane 23 (TIM23), presenilins associated rhomboid-like protein (PARL), PINK1, PARKIN and mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), phosphotyrosine independent ligand for the Lck SH2 domain of 62 kDa (P62), microtubule-associated protein 1 light chain 3 beta (LC3B); the mRNA levels of PINK1 and PARKIN was detected by quantitative polymerase chain reaction; immunoprecipitation assay was used to detect the interaction between PARKIN and Ubiquitin. RESULTS: Resveratrol could inhibit the proliferation of H9C2 cells in a time- and concentration- dependent manner; however, pretreatment with low cytotoxic resveratrol could reduce the H/R-induced increase in cellular ROS levels, alleviate the loss of mitochondrial membrane potential induced by H/R, inhibit H/R-induced apoptosis of H9C2 cells, and protect the mitochondrial structure and respiratory chain of H9C2 cells from H/R damage. Resveratrol could further increase the levels of p62, PINK1, PARKIN protein, the expression of PINK1, PARKIN mRNA and the ratio of LC3BII/LC3B I in H/R-induced H9C2 cells, inhibit the interaction between PARKIN and Ubiquitin in H/R-induced H9C2 cells, and further reduce the expression of TOM20, TIM23, PARL, Mfn1 and Mfn2 protein in H/R-induced H9C2 cells. The effect of resveratrol is consistent with that of autophagy activator on H/R-induced H9C2 cells. CONCLUSIONS: Resveratrol can protect H9C2 cells from H/R injury, which may be related to resveratrol promoting mitochondrial autophagy by activating PINK1/PARKIN signaling pathway. (C) 2022 JTCM. All rights reserved.

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