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首页> 外文期刊>American Journal of Translational Research >Schizandrin A protects against cerebral ischemia-reperfusion injury by suppressing inflammation and oxidative stress and regulating the AMPK/Nrf2 pathway regulation
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Schizandrin A protects against cerebral ischemia-reperfusion injury by suppressing inflammation and oxidative stress and regulating the AMPK/Nrf2 pathway regulation

机译：五味子素A通过抑制炎症和氧化应激并调节AMPK / Nrf2通路的调节作用来预防脑缺血再灌注损伤

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Inflammation and oxidative stress are considered major factors in the pathogenesis of ischemic stroke. Increasing evidence has demonstrated that Schizandrin A (Sch A), a lignin compound isolated from Schisandra chinesnesis, exhibits prominent anti-inflammatory and antioxidant activities. In this study, we investigated the anti-inflammatory and antioxidant effects of Sch A against cerebral ischemia/reperfusion (I/R) injury as well as the underlying molecular mechanisms. Sch A treatment significantly improved the neurological score and reduced infarct volume 24 h after reperfusion. It dose-dependently inhibited the expression of cyclooxygenase-2 and inducible nitric oxide synthase, reduced the release of pro-inflammatory cytokines (tumor necrosis factor-α interleukin [IL]-1β and IL-6), and increased anti-inflammatory cytokines (transforming growth factor-β and interleukin-10). Furthermore, it increased the activity of superoxide dismutase and catalase, decreased reactive oxygen species production and 4-hydroxynonenal and 8-hydroxy-2’-deoxyguanosine levels. Transcription of nuclear factor erythroid 2-related factor 2 (Nrf2) and downstream genes (heme oxygenase-1 and NAD[P]H: quinone oxidoreductase 1) increased. Knockdown of Nrf2 by siRNA inhibited the neuroprotective effects of Sch A. In addition, Sch A increased phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) both in vivo and in vitro. Activation of the Nrf2 pathway as well as the protective effects of Sch A in an oxygen and glucose deprivation-induced injury model was abolished by AMPK knockdown. Our study indicates that Sch A protects against cerebral I/R injury by suppressing inflammation and oxidative stress, and that this effect is regulated by the AMPK/Nrf2 pathway.
机译：炎症和氧化应激被认为是缺血性中风发病的主要因素。越来越多的证据表明，从五味子五味子中分离出的木质素化合物五味子素A（Sch A）具有显着的抗炎和抗氧化活性。在这项研究中，我们研究了Sch A对脑缺血/再灌注（I / R）损伤的抗炎和抗氧化作用以及潜在的分子机制。 Sch A治疗可显着改善神经学评分，并在再灌注后24 h减少梗死体积。它剂量依赖性地抑制了环氧合酶2和诱导型一氧化氮合酶的表达，减少了促炎细胞因子（肿瘤坏死因子-α白介素[IL]-1β和IL-6）的释放，并增加了抗炎细胞因子（转化生长因子-β和白介素-10）。此外，它增加了超氧化物歧化酶和过氧化氢酶的活性，降低了活性氧的产生以及4-羟基壬烯醛和8-羟基-2′-脱氧鸟苷的水平。核因子红系2相关因子2（Nrf2）和下游基因（血红素加氧酶-1和NAD [P] H：醌氧化还原酶1）的转录增加。 siRNA抑制Nrf2抑制了Sch A的神经保护作用。此外，Sch A在体内和体外均增强了磷酸腺苷单磷酸激活的蛋白激酶（AMPK）的磷酸化。 AMPK敲除消除了Nrf2途径的激活以及Sch A在氧和葡萄糖剥夺引起的损伤模型中的保护作用。我们的研究表明，Sch A通过抑制炎症和氧化应激来预防脑I / R损伤，并且该作用受AMPK / Nrf2途径调节。

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