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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Exogenous hydrogen sulfide attenuates cerebral ischemia-reperfusion injury by inhibiting autophagy in mice
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Exogenous hydrogen sulfide attenuates cerebral ischemia-reperfusion injury by inhibiting autophagy in mice

机译：外源硫化氢通过抑制小鼠的自噬抑制脑缺血再灌注损伤

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摘要

Hydrogen sulfide (H2S), the third gas transmitter, has been proven to be neuroprotective in cerebral ischemic injury, but whether its effect is mediated by regulating autophagy is not yet clear. The present study was undertaken to explore the underlying mechanisms of exogenous H2S on autophagy regulation in cerebral ischemia. The effects and its connection with autophagy of NaHS, a H2S donor, were observed through neurological deficits and cerebral infarct volume in middle cerebral artery occlusion (MCAO) mice; autophagy-related proteins and autophagy complex levels in the ischemic hemisphere were detected with Western blot assay. Compared with the model group, NaHS significantly decreased infarct volume and improved neurological deficits; rapamycin, an autophagy activator, abolished the effect of NaHS; NaHS decreased the expression of LC3-II and up-regulated p62 expression in the ischemic cortex 24 h after ischemia. However, NaHS did not significantly influence Beclin-1 expression. H2S has a neuroprotective effect on ischemic injury in MCAO mice; this effect is associated with its influence in down-regulating autophagosome accumulation.
机译：硫化氢（H2S），第三燃气发射器已被证明是在脑缺血性损伤中进行神经保护，但其效果是否通过调节自噬介导尚不清楚。本研究探讨了外源H2S对脑缺血中自噬调节的潜在机制。通过中脑动脉闭塞（MCAO）小鼠的神经系统缺陷和脑梗塞体积观察到NaHs的效果及其与NaHS自噬的联系;用Western印迹测定检测缺血半球中的自噬相关蛋白和自噬复合物水平。与模型组相比，NAHs显着降低了梗塞体积和改善的神经学赤字;雷帕霉素，一种自噬活性剂，废除了Nahs的效果;在缺血后，Nahs降低了LC3-II和上调P62表达的表达和上调的P62表达。然而，Nahs没有显着影响Becin-1表达。 H2S对MCAO小鼠缺血性损伤具有神经保护作用;这种效果与其对下调自噬体积累的影响有关。

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