期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 44, 期 1, 页码 279-292出版社
KARGER
DOI: 10.1159/000484680
关键词
Propofol; Caveolin-3; Ischemia-reperfusion; Diabetes; Mitochondrial-dependent apoptosis
资金
- National Natural Science Foundation of China (NSFC) [81270899, 81670770]
- Science and Technology Project Foundation of Guangdong Province, China [2013B031800015]
- Natural Science foundation of Hubei Province [2014CFC1028]
- Research Grants Council (RGC)/GRF [17123915M]
Background/Aims: Hearts from diabetic subjects are susceptible to myocardial ischemia reperfusion (I/R) injury. Propofol has been shown to protect against myocardial I/R injury due to its antioxidant properties while the underlying mechanism remained incompletely understood. Thus, this study aimed to determine whether or not propofol could attenuate myocardial I/R injury by attenuating mitochondrial dysfunction/damage through upregulating Caveolin (Cav)-3 under hyperglycemia. Methods: Cultured rat cardiomyocyte H9C2 cells were subjected to hypoxia/reoxygenation (H/R) in the absence or presence of propofol under high glucose (HG), and cell viability, lactate dehydrogenase (LDH) and mitochondrial viability as well as creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and intracellular adenosine triphosphate (ATP) content were measured with colorimetric Enzyme-Linked Immunosorbent Assays. Intracellular levels of oxidative stress was assessed using 2,7-dichlorodihydrofluorescein diacetate (DCF-DA) fluorescent staining and mitochondrial-dependent apoptosis was assessed by detecting mitochondrial membrane potential and the activation of apoptotic caspases 3 and 9. Results: Exposure of cells to HG without or with H/R both significantly increased cell injury, cell apoptosis and enhanced oxidative stress that were associated with mitochondrial dysfunction and decreased Cav-3 protein expression. All these changes were further exacerbated following H/R under HG. Administration of propofol at concentrations from 12.5 to 50 mu M but not 100 mu M significantly attenuated H/R injury that was associated with increased Cav-3 expression and activation of the prosurvival proteins Akt and STAT3 with the optimal protective effects seen at 50 mu M of propofol (P25). The beneficial effects of propofol(P25) were abrogated by Cav-3 disruption with beta-methyl-cyclodextrin. Conclusion: Propofol counteracts cardiomyocyte H/R injury by attenuating mitochondrial damage and improving mitochondrial biogenesis through upregulating Cav-3 during hyperglycemia. (c) 2017 The Author(s) Published by S. Karger AG, Basel
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