期刊
CELL BIOLOGY AND TOXICOLOGY
卷 28, 期 1, 页码 19-29出版社
SPRINGER
DOI: 10.1007/s10565-011-9202-x
关键词
AMPK; Autophagic cell death; Cardiomyocytes; Hydrogen peroxide; JNK; Oxidative stress; Propofol
资金
- Ministry of Health and Welfare, Republic of Korea [A080403]
- National Research Foundation of Korea
- Korean government [NRF-2009-0071600, R13-2005-012-02002-0]
- Korea Health Promotion Institute [A080403] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [R13-2005-012-02002-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Autophagy, a self-eating process, is responsible for degradation of long-lived proteins and damaged cellular proteins/organelles. Double-membrane autophagosomes, formed during the process, engulf proteins/organelles and fuse with lysosomes to degrade the contents. It is important to maintain cell homeostasis and many physiological processes including cellular responses to oxidative stress. Oxidative stress induced by myocardial infarction is a major factor of heart failures. In this study, we examined how propofol modulates hydrogen peroxide (H2O2)-induced autophagic cell death in H9c2 cardiomyocytes. H2O2 dramatically induced cell death, which was similarly reduced in the presence of either propofol or autophagy inhibitors (e. g., wortmannin), suggesting that propofol has a protective effect in H2O2-induced autophagic cell death. Acidic autophagic vacuoles were elevated in H2O2-treated H9c2 cells, but they were largely decreased in the presence of propofol. Furthermore, many autophagy-related proteins such as LC3-II, ATG proteins, p62, AMPK, and JNK were activated in H2O2-treated H9c2 cells and were significantly deactivated in the presence of propofol. These results show that propofol regulates oxidative stress-induced autophagic cell death in cardiomyocytes. We further suggest that propofol can act as a cardioprotectant in heart diseases.
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