[Objective] To explore the change of the expression of Fas protein in rat focal cerebral ischemia reperfusion injury at different time points and the effect of d1 3n butylphthalide(NBP). [Methods] Eighty four Wistar rats were randomly divided into sham operation group, ischemia reperfusion group and NBP treatment group. All experiment groups were divided into 6h subgroup, 12h subgroup and 24h subgroup after ischemia reperfusion. Modified thread bolt method was used to establish the rat model of focal brain ischemia reperfu sion. Pathological HE staining was used to observe the morphological change. The apoptosis cells were detec ted by TUNEL method. Western blotting was used to detect the expression of Fas protein. [Results] The ex pression of Fas protein in cytoplasm 6h after cerebral ischemia reperfusion increased, and was up to the most at 24h after cerebral ischemia reperfusion. Fas protein in ischemia reperfusion group was strongly positively ex pressed, while the expression of Fas protein in NBP group was low. There were significant differences among 3 groups. [Conclusion] NBP can protect the necrosis and apoptosis of nerve cells induced by focal cerebral is chemia reperfusion in rats. It may be correlated with the protection of neurons through inhibiting the releasing of Fas protein.%[目的]探讨Fas蛋白在大鼠局灶脑缺血再灌注损伤后不同时间点的表达变化及丁苯酞对其的影响.[方法]84只Wistar大鼠随机分为假手术组、缺血再灌注组、丁苯酞治疗组.各实验组又分为缺血再灌注后6h、12h、24h亚组.采用改良的线栓法制作大鼠局灶性脑缺血再灌注模型,病理学HE染色观察形态学变化,TUNEL法原位检测凋亡细胞,Western免疫印迹检测Fas蛋白水平的表达.[结果]脑缺血再灌注损伤6h后胞浆中Fas蛋白表达增多,24 h达高峰.缺血再灌注组中Fas蛋白呈强阳性表达,丁苯酞治疗组中Fas蛋白阳性表达较弱,三组比较差异有统计学意义.[结论]丁苯酞对大鼠局灶性脑缺血再灌注损伤导致的神经细胞坏死和凋亡具有良好的保护作用,其可能是通过抑制Fas蛋白的释放起到保护神经元的作用.
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