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首页> 外文期刊>FEBS Open Bio >Sodium hydrosulfide attenuates cerebral ischemia/reperfusion injury by suppressing overactivated autophagy in rats
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Sodium hydrosulfide attenuates cerebral ischemia/reperfusion injury by suppressing overactivated autophagy in rats

机译：硫化氢钠通过抑制大鼠过度自噬而减轻脑缺血/再灌注损伤

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Ischemic stroke is a leading cause of death and disability worldwide, and autophagy may be involved in the pathological process of cerebral ischemia/reperfusion injury. Hydrogen sulfide (H2S) is an endogenous gasotransmitter with protective effects against multiple diseases. Here, we tested the effect of H2S on cerebral ischemia/reperfusion injury in rats. Sodium hydrosulfide (NaHS), an H2S donor, improved neurological function and reduced the size of the infarcts induced by transient middle cerebral artery occlusion (MCAO) followed by reperfusion in rats. NaHS treatment reduced the lactate dehydrogenase (LDH) activity in the serum (a marker of cellular membrane integrity) and the expression of cleaved caspase‐3 (a marker for apoptosis) in the brains of MCAO rats. We also found that autophagy was overactivated in the brains of MCAO rats, as indicated by an increased ratio of LC3 II to I, decreased expression of p62, and transmission electron microscope detection. NaHS treatment significantly inhibited the autophagic activity in the brains of MCAO rats. Furthermore, PC12 cells were subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) to mimic MCAO in vitro. We found that NaHS treatment reduced cellular injury and suppressed overactivated autophagy induced by OGD/R in PC12 cells. An autophagy stimulator (rapamycin) eliminated the protective effect of NaHS against LDH release and caspase‐3 activity induced by OGD/R in PC12 cells. An autophagy inhibitor (3‐methyladenine, 3‐MA) also reduced the cellular injury induced by OGD/R in PC12 cells. In conclusion, the results indicate that overactivated autophagy accelerates cellular injury after MCAO in rats and that exogenous H2S attenuates cerebral ischemia/reperfusion injury via suppressing overactivated autophagy in rats.
机译：缺血性中风是全球死亡和残疾的主要原因，自噬可能参与脑缺血/再灌注损伤的病理过程。硫化氢（H2S）是一种内源性气体递质，对多种疾病具有保护作用。在这里，我们测试了H2S对大鼠脑缺血/再灌注损伤的作用。硫化氢钠（NaHS）是H2S的供体，改善了神经功能，并减小了短暂性脑中动脉闭塞（MCAO）继而引起的大鼠再灌注引起的梗塞面积。 NaHS处理降低了MCAO大鼠大脑中血清乳酸脱氢酶（LDH）的活性（细胞膜完整性的标志）和caspase-3裂解的表达（凋亡的标志）。我们还发现，自噬在MCAO大鼠的大脑中被过度激活，如LC3 II与I的比例增加，p62的表达降低以及透射电子显微镜检测所表明的。 NaHS处理显着抑制MCAO大鼠大脑中的自噬活性。此外，对PC12细胞进行氧-葡萄糖剥夺/复氧（OGD / R），以在体外模拟MCAO。我们发现，NaHS处理可减少PC12细胞中OGD / R诱导的细胞损伤并抑制过度活化的自噬。自噬刺激物（雷帕霉素）消除了NaHS对PC12细胞中OGD / R诱导的LDH释放和caspase-3活性的保护作用。自噬抑制剂（3-甲基腺嘌呤，3-MA）也减少了PC12细胞中OGD / R诱导的细胞损伤。总之，结果表明，过度激活的自噬会加速大鼠MCAO后的细胞损伤，而外源性H2S会通过抑制过度激活的自噬而减轻脑缺血/再灌注损伤。

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