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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：外源性硫化氢通过抑制小鼠自噬减轻脑缺血再灌注损伤

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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）是第三种气体传送剂，已被证明在脑缺血性损伤中具有神经保护作用，但尚不清楚其作用是否由调节自噬介导。本研究旨在探讨外源性硫化氢对脑缺血自噬调控的潜在机制。通过中脑动脉闭塞（MCAO）小鼠的神经功能缺损和脑梗死体积，观察到了H2S供体NaHS的自噬作用及其影响。用蛋白质印迹法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显着减少了梗塞体积并改善了神经功能缺损。雷帕霉素（一种自噬激活剂）取消了NaHS的作用; NaHS降低缺血24 h后缺血皮层中LC3-II的表达，并上调p62的表达。但是，NaHS并未显着影响Beclin-1的表达。 H2S对MCAO小鼠的缺血性损伤具有神经保护作用;这种作用与其下调自噬体积累的影响有关。

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