【摘要】：目的 探討miR-181a在腦缺血損傷與神經(jīng)康復(fù)中的作用機(jī)制。方法 構(gòu)建腦缺血大鼠模型和miR-181a過表達(dá)載體,通過尾靜脈注射促進(jìn)腦缺血大鼠腦組織中miR-181a的表達(dá)。RT-PCR檢測(cè)24 h后腦組織miR-181a的表達(dá)水平。Tunel檢測(cè)海馬區(qū)細(xì)胞凋亡情況。對(duì)腦缺血大鼠模型進(jìn)行神經(jīng)功能評(píng)分。Western印跡檢測(cè)大鼠腦組織中白細(xì)胞介素(IL)-1β、腫瘤壞死因子(TNF)-α、IL-6的表達(dá)水平。結(jié)果 腦缺血處理的大鼠缺血組、對(duì)照組、促進(jìn)組的miR-181a水平均明顯高于正常組,促進(jìn)組高于對(duì)照組和缺血組(P0.01),對(duì)照組和缺血組無顯著差異(P0.05)。尾靜脈注射的r AAV-miR-181a載體可以有效促進(jìn)大鼠腦組織中miR-181a的表達(dá)。Tunel結(jié)果顯示,促進(jìn)組中腦組織海馬區(qū)的陽性細(xì)胞比例高于對(duì)照組。促進(jìn)腦缺血大鼠miR-181a的表達(dá),腦組織中細(xì)胞凋亡率增高。促進(jìn)組大鼠神經(jīng)功能評(píng)分明顯高于對(duì)照組(P0.05),大鼠腦組織中IL-1β、TNF-α、IL-6蛋白表達(dá)水平均明顯高于對(duì)照組(P0.01)。結(jié)論 miR-181a在腦缺血組織中過表達(dá),可以促進(jìn)腦組織細(xì)胞凋亡和炎癥的發(fā)生,加重神經(jīng)損傷的嚴(yán)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)-偽) 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- 偽 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.
【作者單位】： 西南醫(yī)科大學(xué)附屬醫(yī)院康復(fù)醫(yī)學(xué)科;
【分類號(hào)】：R743.3

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