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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >TGF-beta improves myocardial function and prevents apoptosis induced by anoxia-reoxygenation, through the reduction of endoplasmic reticulum stress
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TGF-beta improves myocardial function and prevents apoptosis induced by anoxia-reoxygenation, through the reduction of endoplasmic reticulum stress

机译：TGF-β可通过减少内质网应激来改善心肌功能并防止缺氧复氧诱导的细胞凋亡

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Background: Transforming growth factor-beta (TGF-beta) is known for its role in ventricular remodeling, inflammatory response, cell survival, and apoptosis. However, its role in improving myocardial function in rat hearts subjected to ischemia-reperfusion (I/R) and protecting against apoptosis induced in cardiomyocytes by anoxia-reoxygenation (A/R) has not been elucidated. This study investigated the protective effects and molecular mechanisms of TGF-beta on myocardial function and cardiomyocyte apoptosis. Methods and results: We used TUNEL staining, we tested cell viability, and we measured mitochondrial membrane potential and levels of mitochondrial ROS after 6 h of simulated anoxia together with various durations of simulated reoxygenation in H9c2 cells. We further observed the contractile function in rat hearts after they were subjected to 30 min global ischemia and 180 min reperfusion. Pretreatment with TGF-beta markedly inhibited apoptosis in H9c2 cells, as evidenced by increased cell viability and decreased numbers of TUNEL-positive cells, maintained mitochondrial membrane potential, and diminished mitochondrial production of reactive oxygen species (ROS). These changes were associated with the inhibition of endoplasmic reticulum (ER) stress-dependent markers of apoptosis (GRP78, CHOP, caspase-12, and JNK), and the modulation of the expression of Bcl2/Bax. Furthermore, TGF-beta improved I/R-induced myocardial contractile dysfunction. All of these protective effects were concentration-dependent. Conclusion: Our results show that TGF-beta prevents A/R-induced apoptosis of cardiomyocytes and improves myocardial function in rat hearts injured by I/R.
机译：背景：转化生长因子-β（TGF-β）以其在心室重构，炎症反应，细胞存活和凋亡中的作用而闻名。然而，尚未阐明其在改善缺血/再灌注（I / R）大鼠心脏的心肌功能以及防止由缺氧-再充氧（A / R）引起的心肌细胞凋亡中的作用。本研究探讨了TGF-β对心肌功能和心肌细胞凋亡的保护作用及其分子机制。方法和结果：我们使用TUNEL染色，测试了细胞活力，并在模拟缺氧6 h以及不同时间的H9c2细胞中测量了线粒体膜电位和线粒体ROS水平。我们进一步观察了大鼠心脏经历30分钟的整体缺血和180分钟的再灌注后的收缩功能。 TGF-β预处理可显着抑制H9c2细胞凋亡，这可通过增加细胞活力和减少TUNEL阳性细胞数量，保持线粒体膜电位以及减少线粒体活性氧（ROS）来证明。这些变化与内质网（ER）应激依赖的凋亡标记（GRP78，CHOP，caspase-12和JNK）的抑制以及Bcl2 / Bax表达的调节有关。此外，TGF-β可改善I / R引起的心肌收缩功能障碍。所有这些保护作用都是浓度依赖性的。结论：我们的研究结果表明，TGF-β可以防止A / R诱导的心肌细胞凋亡，并改善I / R损伤大鼠心脏的心肌功能。

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