Sevoflurane postconditioning (SPostC) is proved effective against myocardial cardioprotection injury. It has been reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. The mechanism of sevoflurane to protect cardiomyocytes via HSP70 is still understood. We aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry, cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress, and inflammation and increased viability of HR-induced cardiomyocytes. Besides, SPostC down-regulated Bax and Cleaved caspase-3 levels, while SPostC up-regulated Bcl-2, CDK-4, CyclinD1, and HSP70 levels. SiHSP70 had the opposite effect which SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrated that SPostC reduced the HR injury of cardiomyocytes by inducing HSP70 expression.

中文翻译：

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七氟烷后处理通过上调热休克蛋白减少心肌细胞的缺氧/复氧损伤 70。

七氟醚后处理 (SPostC) 被证明对心肌心脏保护损伤有效。据报道，七氟醚可诱导热休克蛋白 70 (HSP70)，其在心肌细胞缺氧/复氧 (HR) 损伤中起着至关重要的作用。七氟醚通过 HSP70 保护心肌细胞的机制尚不清楚。我们旨在研究SPostC诱导HSP70表达以减轻心肌细胞HR损伤的相关机制。HR心肌细胞模型建立后，转染或未转染HSP70 siRNA（siHSP70）的细胞在复氧期间用七氟醚处理。通过比色法检测乳酸脱氢酶（LDH）水平，通过MTT和流式细胞术检测细胞活力和细胞凋亡。逆转录定量聚合酶链反应 (RT-qPCR) 和蛋白质印迹法用于检测 HSP70、细胞凋亡、细胞周期相关因子、iNOS 和 Cox-2 的表达。酶联免疫吸附测定 (ELISA) 用于测量丙二醛 (MDA) 和超氧化物歧化酶 (SOD)。SPostC 减少细胞凋亡、细胞损伤、氧化应激和炎症，并增加 HR 诱导的心肌细胞的活力。此外，SPostC 下调 Bax 和 Cleaved caspase-3 水平，而 SPostC 上调 Bcl-2、CDK-4、CyclinD1 和 HSP70 水平。SiHSP70 具有与 SPostC 对 HR 诱导的心肌细胞相反的作用。此外，siHSP70 进一步逆转了 SPostC 对细胞凋亡、细胞损伤、氧化应激、炎症、活力和 HSP70、细胞凋亡-、和 HR 诱导的心肌细胞中的细胞周期相关因子。总之，本研究表明 SPostC 通过诱导 HSP70 表达来减少心肌细胞的 HR 损伤。