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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >miR-221 Exerts Neuroprotective Effects in Ischemic Stroke by Inhibiting the Proinflammatory Response
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miR-221 Exerts Neuroprotective Effects in Ischemic Stroke by Inhibiting the Proinflammatory Response

机译：MiR-221通过抑制促炎反应来施加缺血性卒中的神经保护作用

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Background: Ischemic stroke is clearly affected by microRNAs (miRNAs) due to dysfunction of their regulatory networks. Our clinical data confirmed decreased miR-221 levels in plasma collected from patients with acute ischemia compared with plasma from healthy controls. Therefore, we further aimed to demonstrate the regulatory mechanisms by which miR-221 exerts its neuroprotective effects in acute ischemic brain injury. Methods: Middle cerebral artery occlusion (MCAO) was used to establish focal cerebral ischemia in adult male C57BL /6 mice. A miR-221 mimic or a negative mimic control was injected by intracerebroventricular administration 24 h prior to MCAO. After 48 h, cerebral infarction volume and neurological scores were calculated, and to determine the extent of neuroprotection by miR-221, neurobehavioral tests were performed. Quantitative real-time PCR, ELISA, and flow cytometry were also performed to identify the expression of inflammation-related cytokines and chemokines as well as infiltration/activation of various immune cells in the brain. Results: The results showed that MCAO mice treated with a miR-221 mimic exhibited significantly decreased cerebral infarction volume and increased amelioration of behavioral deficits. Moreover, the expression of proinflammatory cytokines (TNE-alpha, MCP-1, VCAM-1, and IL-6) and chemokines (CCL2 and CCL3) was significantly decreased in the miR-221 mimic-treated group. In addition, the flow cytometry data showed that macrophage infiltration and microglial activation were blocked by miR-221 treatment. Conclusion: our results indicate that miR-221 could decrease brain damage in the setting of acute ischemic stroke by inhibiting the proinflammatory response, which furthered our understanding of the molecular basis of miR-221 and provided a new potential therapeutic target for the treatment of ischemic stroke.
机译：背景：由于microRNA（miRNAs）调节网络的功能障碍，缺血性中风明显受到其影响。我们的临床数据证实，与健康对照组相比，急性缺血患者血浆中的miR-221水平降低。因此，我们进一步旨在证明miR-221在急性缺血性脑损伤中发挥神经保护作用的调节机制。方法：采用大脑中动脉闭塞（MCAO）建立成年雄性C57BL/6小鼠局灶性脑缺血模型。在MCAO前24小时，通过侧脑室注射miR-221模拟物或阴性模拟物对照。48小时后，计算脑梗死体积和神经功能评分，并进行神经行为测试以确定miR-221的神经保护程度。还进行了定量实时PCR、ELISA和流式细胞术，以确定炎症相关细胞因子和趋化因子的表达，以及各种免疫细胞在大脑中的浸润/激活。结果：结果显示，用miR-221模拟物治疗的MCAO小鼠表现出显著的脑梗死体积减少和行为缺陷的改善。此外，在miR-221模拟治疗组中，促炎细胞因子（TNEα、MCP-1、VCAM-1和IL-6）和趋化因子（CCL2和CCL3）的表达显著降低。此外，流式细胞术数据显示，miR-221治疗可阻断巨噬细胞浸润和小胶质细胞激活。结论：我们的研究结果表明，miR-221可以通过抑制促炎症反应来减轻急性缺血性卒中时的脑损伤，这进一步加深了我们对miR-221分子基础的理解，并为缺血性卒中的治疗提供了一个新的潜在治疗靶点。

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