miR-181a在脑缺血神经损伤与神经康复中的作用
发布时间：2018-08-09 18:48
【摘要】：目的 探讨miR-181a在脑缺血损伤与神经康复中的作用机制。方法 构建脑缺血大鼠模型和miR-181a过表达载体,通过尾静脉注射促进脑缺血大鼠脑组织中miR-181a的表达。RT-PCR检测24 h后脑组织miR-181a的表达水平。Tunel检测海马区细胞凋亡情况。对脑缺血大鼠模型进行神经功能评分。Western印迹检测大鼠脑组织中白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、IL-6的表达水平。结果 脑缺血处理的大鼠缺血组、对照组、促进组的miR-181a水平均明显高于正常组,促进组高于对照组和缺血组(P0.01),对照组和缺血组无显著差异(P0.05)。尾静脉注射的r AAV-miR-181a载体可以有效促进大鼠脑组织中miR-181a的表达。Tunel结果显示,促进组中脑组织海马区的阳性细胞比例高于对照组。促进脑缺血大鼠miR-181a的表达,脑组织中细胞凋亡率增高。促进组大鼠神经功能评分明显高于对照组(P0.05),大鼠脑组织中IL-1β、TNF-α、IL-6蛋白表达水平均明显高于对照组(P0.01)。结论 miR-181a在脑缺血组织中过表达,可以促进脑组织细胞凋亡和炎症的发生,加重神经损伤的严重程度。
[Abstract]:Objective to investigate the mechanism of miR-181a in cerebral ischemic injury and neurorehabilitation. Methods the rat model of cerebral ischemia and the overexpression vector of miR-181a were constructed. The expression of miR-181a in brain tissue was detected by tail vein injection. RT-PCR was used to detect the expression level of miR-181a in brain tissue after 24 h. Tunel was used to detect the apoptosis of hippocampal cells. The expression of interleukin-1 尾 (IL) 尾) and tumor necrosis factor (TNF)-伪) IL-6 in brain tissue of rats with cerebral ischemia was detected by Western blot. Results the levels of miR-181a in ischemic group, control group and promoting group were significantly higher than those in normal group (P0.01), but there was no significant difference between control group and ischemic group (P0.05). R AAV-miR-181a vector injected via tail vein could effectively promote the expression of miR-181a in rat brain. The results showed that the proportion of positive cells in hippocampal area of the promoting group was higher than that in the control group. Promote the expression of miR-181a in cerebral ischemia rats, and increase the apoptosis rate in brain tissue. The neurologic function score of the promoting group was significantly higher than that of the control group (P0.05), and the expression of IL-1 尾 -TNF- 伪 IL-6 protein was significantly higher in the brain tissue than that in the control group (P0.01). Conclusion overexpression of miR-181a in cerebral ischemic tissue can promote apoptosis and inflammation of brain tissue and aggravate the severity of nerve injury.
【作者单位】： 西南医科大学附属医院康复医学科;
【分类号】：R743.3
本文编号：2174977
[Abstract]:Objective to investigate the mechanism of miR-181a in cerebral ischemic injury and neurorehabilitation. Methods the rat model of cerebral ischemia and the overexpression vector of miR-181a were constructed. The expression of miR-181a in brain tissue was detected by tail vein injection. RT-PCR was used to detect the expression level of miR-181a in brain tissue after 24 h. Tunel was used to detect the apoptosis of hippocampal cells. The expression of interleukin-1 尾 (IL) 尾) and tumor necrosis factor (TNF)-伪) IL-6 in brain tissue of rats with cerebral ischemia was detected by Western blot. Results the levels of miR-181a in ischemic group, control group and promoting group were significantly higher than those in normal group (P0.01), but there was no significant difference between control group and ischemic group (P0.05). R AAV-miR-181a vector injected via tail vein could effectively promote the expression of miR-181a in rat brain. The results showed that the proportion of positive cells in hippocampal area of the promoting group was higher than that in the control group. Promote the expression of miR-181a in cerebral ischemia rats, and increase the apoptosis rate in brain tissue. The neurologic function score of the promoting group was significantly higher than that of the control group (P0.05), and the expression of IL-1 尾 -TNF- 伪 IL-6 protein was significantly higher in the brain tissue than that in the control group (P0.01). Conclusion overexpression of miR-181a in cerebral ischemic tissue can promote apoptosis and inflammation of brain tissue and aggravate the severity of nerve injury.
【作者单位】： 西南医科大学附属医院康复医学科;
【分类号】：R743.3
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1 邓镇;miR-497和过氧化物酶增殖体激活受体δ/β对脑缺血神经损伤机制的调控研究[D];南方医科大学;2010年
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