摘要
目的研究生长停滞特异性蛋白6(Gas 6)对Wistar大鼠局灶性脑缺血再灌注损伤的影响,探讨其与PI3K/Akt通路的关系。方法线栓法制作大鼠局灶性脑缺血再灌注模型,将大鼠随机分成4组:假手术组(Sham组)、缺血再灌注组(I/R组)、Gas6预处理组(Gas6组)、Gas6预处理联合PI3K抑制剂Wortmannin组(Gas6+W组)。按Zea-Longa 5分制法测定各组神经功能评分,干湿重法测定脑组织含水量、TTC染色测定脑梗死面积、Western-blot法检测脑组织p-Akt的蛋白表达。结果 I/R组较Sham组神经功能缺损、脑含水量和梗死区均增加,p-Akt表达上调;Gas6组较I/R组,神经功能缺血损伤、脑含水量和梗死面积显著减少,p-Akt表达进一步上调;而给与PI3K抑制剂后,Gas6+W组与Gas6组比较,神经功能缺损、脑含水量和梗死面积显著增加,p-Akt的表达显著下调。结论 Gas6对于大鼠脑缺血再灌注损伤具有保护作用,可能与激活PI3K/Akt信号通路相关。
Objective To study the effect of growth arrest specific protein 6（Gas6） preconditioning on PI3K/AKT in focal cerebral ischemic reperfusion injm7 of Wistar rats. Methods The rat focal cerebral ischemia reperfusion injury model was prepared by suture method, rats were randomly divided into 4 groups： Sham grnup, isehemia reperfusion group （I/R group）, Gas6 group, Gas6＋ P13K inhibitor Wortmannin group（Gas6＋W group）. The neurological scores were determined by Zea-Longa 5＇s method, brain water content was determined by dry-wet weight method, brain infarction area was delermined by TTC staining, the expression of p-Akt protein was detemfined by Western-blot. Results The scores of neural fimetion, brain water content and the infarct area were obvious increased, the expression level of p-Akt was up-regulated in I/R group than in sham group, but decreased obviously in Gas 6 group than in I/R group except the further upregulated expression level of p-Akt. After treatment with PI3K inhibitor, compared with Gas 6 group, scores of neural function, brain water content and the infarct area were obvious increased, the expression level of p-Akl was downregulated in Gas6＋W group. Conclusion The protective effect of Gas 6 on focal cerebral ischemia reperfusion injury mighl be related to the activation of PI3K/Akt signal pathway.
出处
《解剖科学进展》
2016年第4期408-410,415,共4页
Progress of Anatomical Sciences
基金
辽宁省科技厅博士启动基金(20131114)
辽宁省教育厅科学技术研究一般项目(L2015535)
沈阳医学院科技基金项目(20133053)
沈阳医学院大学生科研立项(20141035)
