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首页> 外文期刊>Cellular Physiology and Biochemistry >Propofol Through Upregulating Caveolin-3 Attenuates Post-Hypoxic Mitochondrial Damage and Cell Death in H9C2 Cardiomyocytes During Hyperglycemia
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Propofol Through Upregulating Caveolin-3 Attenuates Post-Hypoxic Mitochondrial Damage and Cell Death in H9C2 Cardiomyocytes During Hyperglycemia

机译：丙泊酚通过上调Caveolin-3来减轻高血糖期间低氧后线粒体损伤和H9C2心肌细胞的细胞死亡

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>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 ?μM but not 100 ?μM 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 ?μM of propofol (P25). The beneficial effects of propofol(P25) were abrogated by Cav-3 disruption with ?2-methyl-cyclodextrin. Conclusion: Propofol counteracts cardiomyocyte H/R injury by attenuating mitochondrial damage and improving mitochondrial biogenesis through upregulating Cav-3 during hyperglycemia.
机译：> 背景/目标： 糖尿病患者的心脏容易受到心肌缺血再灌注（I / R）的伤害。由于其抗氧化特性，丙泊酚已被证明可预防心肌I / R损伤，而其潜在机理尚不完全清楚。因此，本研究旨在确定丙泊酚是否可以通过在高血糖下通过上调Caveolin（Cav）-3减轻线粒体功能障碍/损伤来减轻心肌I / R损伤。 方法： 培养的大鼠心肌细胞H9C2细胞在不存在或存在丙泊酚的情况下，在高葡萄糖（HG）下进行缺氧/复氧（H / R），并具有细胞活力，用比色酶联免疫吸附法测定了乳酸脱氢酶（LDH）和线粒体的活力以及肌酸激酶-MB（CK-MB），心肌肌钙蛋白I（cTnI）和细胞内三磷酸腺苷（ATP）的含量。使用2,7-二氯二氢荧光素二乙酸酯（DCF-DA）荧光染色评估细胞内的氧化应激水平，并通过检测线粒体膜电位以及凋亡胱天蛋白酶3和9的活化来评估线粒体依赖性凋亡。 结果： 细胞暴露于无或无H / R的HG均显着增加了细胞损伤，细胞凋亡和氧化应激，这与线粒体功能障碍和Cav-3蛋白表达降低有关。在HG下进行H / R之后，所有这些变化进一步加剧。丙泊酚的给药浓度为12.5至50？μM，而不是100？μM，可显着减轻H / R损伤，这与Cav-3表达增加和生存蛋白Akt和STAT3的激活有关，在50？μM时具有最佳保护作用异丙酚（P25）。丙泊酚（P25）的有益作用被α2-甲基-环糊精的Cav-3破坏所废除。 结论： 异丙酚在高血糖症中通过上调Cav-3来减轻线粒体损伤并改善线粒体生物发生，从而抵消心肌H / R损伤。

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