富氢液通过PI3K通路减轻大鼠脑缺血再灌注损伤

发布时间：2018-09-13 11:05

【摘要】：目的探讨富氢液对大鼠脑缺血再灌注致海马神经元凋亡及PI3K/Akt/FoxO1信号通路表达的影响。方法采用线栓法阻塞大鼠大脑中动脉,建立大鼠局灶性脑缺血/再灌注(I/R)模型,SD大鼠随机分为假手术组(Sham组)、缺血/再灌注组(I/R组)和富氢液处理组(HRS组),每组10只;各组于再灌注后24 h,ELISA检测血清中炎症因子IL-6、TNF-α及IL-1β的变化;HE染色观察海马变化,TUNEL法观察脑组织细胞凋亡情况;Western blot法检测海马p-PI3K、Akt、caspase-3和FoxO1蛋白表达变化。结果与Sham组相比,I/R组锥体细胞排列疏松,大量锥体细胞死亡,海马凋亡细胞增多,血清炎症因子IL-1β、IL-6、TNF-α、表达显著增加(P0.05),脑组织中pPI3K、Akt、caspase-3表达显著升高,FoxO1蛋白降低,两组间比较均具有统计学差异(P0.05);与I/R组相比,HRS组炎症因子显著降低;p-PI3K、Akt、caspase-3表达水平均显著降低,,FoxO1蛋白升高(P0.05)。结论富氢液可以减轻缺血再灌注导致的脑损伤,其机制可能与PI3K/Akt/FoxO1信号通路相关。
[Abstract]:Objective to investigate the effects of hydrogen rich solution on hippocampal neuronal apoptosis and expression of PI3K/Akt/FoxO1 signal pathway after cerebral ischemia reperfusion in rats. Methods Sprague-Dawley rats with focal cerebral ischemia / reperfusion (I / R) were randomly divided into three groups: sham operation group (Sham group), ischemia / reperfusion group (I / R group) and hydrogen rich solution treatment group (HRS group) with 10 rats in each group. The changes of IL-6,TNF- 伪 and IL-1 尾 in serum were detected by Elisa at 24 hours after reperfusion. The changes of hippocampus were observed by HE staining. The apoptosis of brain tissue was observed by Tunel method. The expression of p-PI3KnAktcaspase-3 and FoxO1 protein in hippocampus were detected by Western blot. Results compared with Sham group, the pyramidal cells were loosely arranged, a large number of pyramidal cells died, the number of apoptotic cells in hippocampus increased, the expression of serum inflammatory factor IL-1 尾, IL-6, TNF- 伪, and the expression of pPI3K,Akt,caspase-3 in brain tissue decreased significantly (P0.05). Compared with the I / R group, the inflammatory factors in HRS group significantly decreased the expression level of p-PI3KT AktCaspase-3 and the protein of FoxO1 increased significantly (P0.05). Conclusion Hydrogen-rich solution can attenuate the brain injury induced by ischemia and reperfusion, and its mechanism may be related to the PI3K/Akt/FoxO1 signal pathway.
【作者单位】：中国医科大学实验动物部;
【基金】：国家自然青年科学基金项目(31201758) 中国医科大学新教师基金项目(XZR20160036)
【分类号】：R743.3

【相似文献】