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Shock Wave Therapy Promotes Cardiomyocyte Autophagy and Survival during Hypoxia

机译:冲击波疗法促进缺氧时心肌细胞的自噬和存活

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>Background: Autophagy plays an important role in cardiovascular disease. Controversy still exists regarding the effect of autophagy on ischemic/hypoxic myocardium. Cardiac shock wave therapy (CSWT) is an effective alternative treatment for refractory ischemic heart disease. Whether CSWT can regulate cardiomyocyte autophagy under hypoxic conditions is not clear. We established a myocardial hypoxia model using the H9c2 cell line and performed shock waves (SWs) treatment to evaluate the effect of SW on autophagy. Methods: The H9c2 cells were incubated under hypoxic conditions, and SW treatment was then performed at energies of 0.02, 0.05, or 0.10 mJ/mm2. The cell viability and intracellular ATP level were examined. Western blot analysis was used to assess the expression of LC3B, AMPK, mTOR, Beclin-1, Sirt1, and HIF-1?±. Autophagic vacuoles were visualized by monodansylcadaverine staining. Results: After the 24-hour hypoxic period, cardiomyocyte viability and ATP levels were decreased and autophagy was significantly increased in H9c2 cells. SW treatment with an energy of 0.05 mJ/mm2 significantly increased the cellular viability, ATP level, LC3B-II/I, and number of autophagic vacuoles. In addition, phosphorylated AMPK and Sirt1 were increased and phosphorylated mTOR and HIF-1?± were decreased after SW treatment. Conclusion: SW treatment can potentially promote cardiomyocyte autophagy during hypoxia and protect cardiomyocyte function by regulating the AMPK/mTOR pathway.
机译:> 背景: 自噬在心血管疾病中起着重要作用。自噬对缺血/缺氧心肌的影响仍然存在争议。心脏冲击波疗法(CSWT)是治疗难治性缺血性心脏病的有效替代疗法。目前尚不清楚CSWT是否能在缺氧条件下调节心肌细胞的自噬。我们使用H9c2细胞系建立了心肌缺氧模型,并进行了冲击波(SWs)治疗以评估SW对自噬的影响。 方法: 在低氧条件下孵育H9c2细胞,然后以0.02、0.05或0.10 mJ / mm 2 。检查细胞活力和细胞内ATP水平。使用蛋白质印迹分析来评估LC3B,AMPK,mTOR,Beclin-1,Sirt1和HIF-1α±的表达。通过单丹酰尸胺染色可见自噬泡。 结果: 低氧24小时后,H9c2细胞的心肌细胞活力和ATP水平降低,自噬显着增加。能量为0.05 mJ / mm 2 的SW处理显着提高了细胞活力,ATP水平,LC3B-II / I和自噬泡的数量。此外,SW处理后,磷酸化的AMPK和Sirt1增加,而磷酸化的mTOR和HIF-1α±降低。 结论: SW治疗可能会在缺氧期间促进心肌细胞自噬,并通过调节AMPK / mTOR途径保护心肌细胞功能。

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