Over the years miR-497 has been found to play a vital role in the pathogenesis of neurological diseases, including ischemic stroke. However, its underlying mechanism remains largely unexplored. Here, we used miR-497 agomir (miR-497 agonist), miR-497 antagomir (miR-497 inhibitor) and 3-MA (autophagy inhibitor) to treat ischemic rats (n = 10-12 per group) induced by permanent distal middle cerebral artery occlusion (dMCAO), followed the functional outcome assessment 24 h after dMCAO. We found that treatment of miR-497 antagomir, but not miR-497 angomir, reduced the infarct volume and improved neurological deficits after ischemic stroke, along with upregulation of the autophagy-related protein LC3 expression (mean ± SEM,p < 0.05). While the ischemic rats treated with 3-MA exhibited inhibition of autophagy, which in turn abolished functional recovery as observed in miR-497 antagomir-treated group (p < 0.05). Interestingly, the role of miR-497 in functional recovery in aged ischemic rats was less effective, compared to young adult ischemic rats (p < 0.05). Our data suggest that inhibition of miR-497 could protect cerebral ischemic injury by enhancing autophagy and also age-dependent.

中文翻译：

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抑制miR-497可通过增强年轻和老年大鼠的神经元自噬来改善缺血性中风后的功能结局。

多年来，已发现miR-497在包括缺血性中风在内的神经系统疾病的发病机理中起着至关重要的作用。但是，其基本机制仍未得到充分探索。在这里，我们使用了miR-497 agomir（miR-497激动剂），miR-497 antagomir（miR-497抑制剂）和3-MA（自噬抑制剂）来治疗由永久性远端所致的缺血大鼠（每组10-12只）大脑中动脉闭塞（dMCAO），并在dMCAO后24小时进行功能预后评估。我们发现，miR-497 antagomir而不是miR-497 angomir的治疗减少了缺血性中风后的梗塞体积并改善了神经功能缺损，同时上调了自噬相关蛋白LC3的表达（平均值±SEM，p <0.05）。虽然用3-MA处理的缺血大鼠表现出自噬抑制作用，如在miR-497 antagomir治疗组中观察到的，这反过来消除了功能恢复（p <0.05）。有趣的是，与年轻的成年缺血大鼠相比，miR-497在老年缺血大鼠的功能恢复中的作用较差（p <0.05）。我们的数据表明，抑制miR-497可以通过增强自噬和年龄依赖性来保护脑缺血性损伤。