首页> 美国卫生研究院文献>Aging (Albany NY) >Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway
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Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway

机译:通过SIRT1-FOXO1信号通路抑制自噬电针改善了脑缺血/再灌注损伤

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摘要

Cerebral ischemia/reperfusion (CIR) injury occurs when blood flow is restored in the brain, causing secondary damage to the ischemic tissues. Previous studies have shown that electroacupuncture (EA) treatment contributes to brain protection against CIR injury through modulating autophagy. Studies indicated that SIRT1-FOXO1 plays a crucial role in regulating autophagy. Here we investigated the mechanisms underlying the neuroprotective effect of EA and its role in modulating autophagy the SIRT1-FOXO1 signaling pathway in rats with CIR injury. EA pretreatment at “ ”, “ ” and “ ” acupoints (2/15Hz, 1mA, 30 min/day) was performed for 5 days before the rats were subjected to middle cerebral artery occlusion, and the results indicated that EA pretreatment substantially reduced the Longa score and infarct volume, increased the dendritic spine density and lessened autophagosomes in the peri-ischemic cortex of rats. Additionally, EA pretreatment also reduced the ratio of LC3-II/LC3-I, the levels of Ac-FOXO1 and Atg7, and the interaction of Ac-FOXO1 and Atg7, but increased the levels of p62, SIRT1, and FOXO1. The above effects were abrogated by the SIRT1 inhibitor EX527. Thus, we presume that EA pretreatment elicits a neuroprotective effect against CIR injury, potentially by suppressing autophagy activating the SIRT1-FOXO1 signaling pathway.
机译:脑缺血/再灌注(CIR)损伤发生在大脑中血液流动时,导致缺血组织的二次损害。以前的研究表明,通过调节自噬地,电针(EA)治疗有助于对颅损伤进行脑保护。研究表明,SIRT1-FOXO1在调节自噬中起着至关重要的作用。在这里,我们调查了EA神经保护作用的机制及其在调节CIR损伤大鼠大鼠中的自噬血清菌1-FOXO1信号通路的作用。 EA预处理在“”,“和”“穴位(2/15Hz,1mA,30分钟/天)进行5天,在大鼠进行中脑动脉闭塞之前进行5天,结果表明EA预处理显着降低了Longa得分和梗塞体积,增加树突脊柱密度,并在大鼠的血症缺血皮层中减少自噬体。另外,EA预处理还降低了LC3-II / LC3-I,AC-FOXO1和ATG7水平的比例,以及AC-FOXO1和ATG7的相互作用,但增加了P62,SIRT1和FOXO1的水平。 SIRT1抑制剂EX527废除了上述效果。因此,我们假设EA预处理引发了对CIR损伤的神经保护作用,潜在通过抑制激活SIRT1-FOXO1信号通路的自噬。

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