Abstract：
In the current investigation, we explored the benefits of aucubin against rodent ischemia/reperfusion (I/R) damages in brains and elucidated the role of 5\'-AMP-activated protein kinase (AMPK) in its neuroprotective action. I/R model of brain was established in male three-month-old rats through 2 h of middle cerebral artery occlusion followed by two days of reperfusion. Aucubin boosted phosphorylation of AMPKα in ipsilateral cortex of injured rats. Then, rats were exposed to cerebral I/R damage and received treatment of aucubin and compound C (a well-known AMPK inhibitor). It was found that aucubin administration improved neurological symptom score, decreased infarct volume, and mitigated cerebral edema in injured rats. Aucubin administration upregulated Nrf2 expression and abated oxidative stress in ipsilateral cortex of injured rats. Aucubin administration reduced levels of multiple pro-inflammatory cytokines, suppressed microglial activation and neutrophil infiltration, and promoted M2 polarization in injured rats. More importantly, compound C abolished the neuroprotective, anti-oxidant and inflammation-modulating effects of aucubin in injured rats, at least in part. Therefore, we concluded that activation of AMPK by aucubin alleviated I/R injury in brain through abating oxidative stress and suppressing inflammation, identifying a potential candidate for those patients of ischemic stroke.
摘要：
在目前的调查中,我们探讨了花叶苷对啮齿动物脑缺血/再灌注(I/R)损伤的益处,并阐明了5'-AMP活化蛋白激酶(AMPK)在其神经保护作用中的作用.通过大脑中动脉阻塞2h，再灌注2天，在雄性3月龄大鼠中建立I/R脑模型。在损伤大鼠的同侧皮质中,桃红促进了AMPKα的磷酸化。然后，将大鼠暴露于脑I/R损伤,并接受桃红和化合物C(一种众所周知的AMPK抑制剂)的治疗。发现aucubin给药改善了神经症状评分，梗死体积减少,减轻损伤大鼠的脑水肿。在损伤大鼠的同侧皮质中，应用桃红素上调了Nrf2的表达，减轻了氧化应激。给药桃红降低了多种促炎细胞因子的水平，抑制小胶质细胞活化和中性粒细胞浸润，并促进损伤大鼠的M2极化。更重要的是,化合物C取消了神经保护作用，aucubin对损伤大鼠的抗氧化和炎症调节作用，至少部分。因此,我们得出结论，AMPK的激活通过减轻氧化应激和抑制炎症减轻脑I/R损伤，确定缺血性卒中患者的潜在候选者。
