miR-221在大鼠脑缺血再灌注神经损伤中的作用及其机制

发布时间：2018-02-03 21:24

本文关键词： 脑缺血再灌注损伤微小RNA- 细胞凋亡炎症因子凋亡因子大鼠　出处：《山东医药》2017年40期 　论文类型：期刊论文

【摘要】：目的探讨miR-221在大鼠脑缺血再灌注神经损伤中的作用及其可能机制。方法选择SD大鼠60只,随机分为假手术组、模型组和agomiR-221组,每组20只。模型组、agomiR-221组建立局灶性脑缺血再灌注(MCAO)模型。假手术组仅手术,不阻断血流。成模后agomiR-221组尾静脉注射agomiR-221(miR-221激动剂)80 mg/kg,模型组尾静脉注射等量agomiR-NC,假手术组不予处理。再灌注24 h,各组随机取6只,留取脑组织,采用TTC染色法观察脑梗死体积;另取6只,采用干湿重法计算脑组织含水量;剩余大鼠采用原位末端标记法计算细胞凋亡指数(AI);Real-time PCR法检测脑组织miR-221 mRNA表达;Western blotting法检测脑组织炎症因子IL-1β、TNF-α及凋亡相关蛋白Caspase3表达。结果假手术组和agomiR-221组脑组织miR-211 mRNA相对表达量明显高于模型组,且agomiR-221组高于假手术组(P均0.05)。与假手术组比较,模型组脑梗死体积、脑组织含水量及AI明显升高(P均0.05),而agomiR-221组脑梗死体积、脑组织含水量及AI较模型组明显降低(P均0.05)。与假手术组比较,模型组炎症因子IL-1β、TNF-α以及凋亡相关蛋白Caspse3表达明显升高(P均0.05),而agomiR-221组炎症因子IL-1β、TNF-α以及凋亡相关蛋白Caspse3表达较模型组明显降低(P均0.05)。结论过表达miR-221对大鼠脑缺血再灌注损伤具有神经保护作用,其机制可能与调控炎症反应和细胞凋亡有关。
[Abstract]:Objective to investigate the role of miR-221 in cerebral ischemia-reperfusion nerve injury in rats and its possible mechanism. Methods Sixty SD rats were randomly divided into three groups: sham operation group, model group and agomiR-221 group. A model of focal cerebral ischemia / reperfusion was established in the model group (n = 20). The sham-operated group was operated on only, and the model group (n = 20) was used to establish a model of focal cerebral ischemia / reperfusion (MCAO). No blood flow was blocked. AgomiR-221 group was injected with 80 mg / kg agomiR-221(miR-221 agonist via tail vein, and model group was injected with the same amount of agomiR-NC.The sham operation group was not treated. After 24 hours of reperfusion, 6 rats in each group were randomly selected and the cerebral infarction volume was observed by TTC staining method. Another 6 rats were used to calculate the water content of brain tissue by the method of dry and wet weight. In situ end labeling method was used to calculate apoptosis index and real-time PCR method was used to detect the expression of miR-221 mRNA in brain tissue. Western blotting method was used to detect the expression of inflammatory factor IL-1 尾 TNF- 伪 and apoptosis-related protein Caspase3 in brain tissue. Results miR-211 in brain tissue of sham operation group and agomiR-221 group was detected. The relative expression of mRNA was significantly higher than that of the model group. Compared with sham operation group, the volume of cerebral infarction, water content of brain tissue and AI of model group were significantly higher than that of sham operation group, and the volume of cerebral infarction in agomiR-221 group was higher than that in agomiR-221 group. The water content of brain tissue and AI in the model group were significantly lower than those in the model group (P < 0.05), and were significantly lower than those in the sham operation group. The expression of IL-1 尾 -TNF- 伪 and apoptosis-related protein (Caspse3) in model group was significantly higher than that in model group, while the expression of IL-1 尾 -TNF- 伪 and apoptosis-related protein Caspse3 in agomiR-221 group was significantly lower than that in model group. Conclusion the overexpression of miR-221 can significantly increase the expression of IL-1 尾 -TNF- 伪 and apoptosis-related protein Caspse3 in rats with cerebral ischemia-reperfusion. Injection injury has neuroprotective effect, The mechanism may be related to the regulation of inflammation and apoptosis.
【作者单位】：潍坊医学院附属益都中心医院;
【分类号】：R743
【正文快照】： 脑缺血再灌注损伤(CIR)是指各种原因导致脑组织血流中断,闭塞的脑血管再通后缺血性损伤却进一步加重的现象,是一个由多因素参与的复杂病理生理过程。目前CIR的发生机制主要包括细胞凋亡学说、炎症反应学说、兴奋性氨基酸学说以及自由基学说等[1]。炎症反应和细胞凋亡是诱导CIR

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