p38MAPK介导的Fas/FasL凋亡通路在缺血性脑损伤中的作用研究

目的探讨p38MAPK介导的Fas/FasL凋亡通路在大鼠缺血性脑损伤中的作用。方法①制作大鼠全脑缺血模型,免疫印迹法检测假手术组、脑缺血复灌6 h、12 h、1 d、3 d组p-p38MAPK、p38MAPK蛋白表达。②免疫印迹法检测假手术组、缺血复灌组、溶剂对照组和SB203580组p-p38MAPK、p38MAPK、FasL、Fas和Caspase-3蛋白表达。结果①与假手术组相比,脑缺血再灌注6 h、12 h、1 d、3 d组p-p38MAPK蛋白表达水平逐渐升高,于1 d达高峰(P均<0.05)。②与缺血复灌组和溶剂对照组相比,SB203580组p-p38MAPK、FasL和Caspase-3表达水平显著降低(P均<0.05)。结论 p38MAPK介导的Fas/FasL凋亡通路在缺血性脑损伤中发挥了重要作用。

Study of the Effects of Apoptosis Induced by p38MAPK through Fas/FasL Pathway on Ischemic Brain Injury

Objective Investigate the effects of apoptosis induced by p38MAPK through Fas/FasL pathway on ischemic brain injury in rats. Methods①Making rat model of cerebral ischemia, p-p38MAPK and p38MAPK protein expression were detected by immunoblotting in sham operation group, ischemia-reperfusion（I/R） 6 h, 12 h, 1 d, 3 d group.②p-p38MAPK, p38MAPK, FasL, Fas and Caspase-3 protein expression were detected by immunoblotting 1d after I/R in sham operation group, I/R group, solvent control group and SB203580 group. Results①Compared with the sham operation group, p-p38MAPK protein expression were increased gradually in I/R 6 h, 12 h, 1 d, 3 d group, and reached the peak in I/R 1d group （All 〈0.05）.②Compared with the I/R group and solvent control group, p-p38MAPK、FasL and Caspase-3 protein expression were decreased in SB203580 group （All 〈0.05）. Conclusion Neuronal apoptosis induced by p38MAPK through Fas/FasL pathway played important effects on ischemic brain injury in rats.