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首页> 外文期刊>The European Journal of Neuroscience >Resveratrol prevents CA1 neurons against ischemic injury by parallel modulation of both GSK-3β and CREB through PI3-K/Akt pathways
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Resveratrol prevents CA1 neurons against ischemic injury by parallel modulation of both GSK-3β and CREB through PI3-K/Akt pathways

机译：白藜芦醇通过PI3-K / Akt途径平行调节GSK-3β和CREB来预防CA1神经元抗缺血性损伤

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Accumulating evidence indicates that resveratrol potently protects against cerebral ischemia damage due to its oxygen free radicals scavenging and antioxidant properties. However, cellular mechanisms that may underlie the neuroprotective effects of resveratrol in brain ischemia are not fully understood yet. This study aimed to investigate the potential association between the neuroprotective effect of resveratrol and the apoptosis/survival signaling pathways, in particular the glycogen synthase kinase 3 (GSK-3β) and cAMP response element-binding protein (CREB) through phosphatidylinositol 3-kinase (PI3-K)-dependent pathway. An experimental model of global cerebral ischemia was induced in rats by the four-vessel occlusion method for 10min and followed by different periods of reperfusion. Nissl staining indicated extensive neuronal death at 7days after ischemia/reperfusion. Administration of resveratrol by i.p. injections (30mg/kg) for 7days before ischemia significantly attenuated neuronal death. Both GSK-3β and CREB appear to play a critical role in resveratrol neuroprotection through the PI3-K/Akt pathway, as resveratrol pretreatment increased the phosphorylation of Akt, GSK-3β and CREB in 1h in the CA1 hippocampus after ischemia/reperfusion. Furthermore, administration of LY294002, an inhibitor of PI3-K, compromised the neuroprotective effect of resveratrol and decreased the level of p-Akt, p-GSK-3β and p-CREB after ischemic injury. Taken together, the results suggest that resveratrol protects against delayed neuronal death in the hippocampal CA1 by maintaining the pro-survival states of Akt, GSK-3β and CREB pathways. These data suggest that the neuroprotective effect of resveratrol may be mediated through activation of the PI3-K/Akt signaling pathway, subsequently downregulating expression of GSK-3β and CREB, thereby leading to prevention of neuronal death after brain ischemia in rats.
机译：越来越多的证据表明，白藜芦醇由于其清除氧自由基和抗氧化性能，可以有效地预防脑缺血。但是，尚未完全了解白藜芦醇对脑缺血的神经保护作用的细胞机制。这项研究旨在探讨白藜芦醇的神经保护作用与细胞凋亡/生存信号通路之间的潜在联系，特别是糖原合酶激酶3（GSK-3β）和cAMP反应元件结合蛋白（CREB）通过磷脂酰肌醇3激酶（ PI3-K）依赖性途径。四血管闭塞法诱导大鼠全脑缺血10min，然后再灌注不同时间。 Nissl染色指示缺血/再灌注后7天广泛的神经元死亡。 i.p.给予白藜芦醇缺血前7天注射（30mg / kg）可明显减轻神经元死亡。 GSK-3β和CREB似乎都通过PI3-K / Akt途径在白藜芦醇神经保护中起关键作用，因为白藜芦醇预处理可增加缺血/再灌注后CA1海马中Akt，GSK-3β和CREB的磷酸化。此外，给予PI3-K抑制剂LY294002会损害白藜芦醇的神经保护作用，并降低缺血性损伤后p-Akt，p-GSK-3β和p-CREB的水平。两者合计，结果表明白藜芦醇通过维持Akt，GSK-3β和CREB通路的存活前状态，防止海马CA1神经元延迟死亡。这些数据表明，白藜芦醇的神经保护作用可以通过PI3-K / Akt信号通路的激活来介导，随后下调GSK-3β和CREB的表达，从而预防大鼠脑缺血后神经元死亡。

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