脑缺血再灌流后Fas及FasL在脑内表达的变化和氟桂嗪的抑制作用

EXPRESSION OF FAS AND FASL GENES IN BRAIN AND EFFECT OF FLUNARIZINE ON THESE EXPRESSIONS IN RATS AFTER GLOBAL ISCHEMIA-REPERFUSION

目的 观察全脑缺血再灌流后Fas和FasL基因在脑内表达的变化及氟桂嗪的影响。方法 用大鼠 4血管结扎全脑缺血 30min再灌流模型和免疫组织化学染色法。结果 脑缺血再灌流 6h在皮质及海马区即出现Fas表达阳性细胞 ,2 4～ 48h时达高峰 ;FasL则在 12h后出现 ,48～ 72h时达到高峰。ip氟桂嗪 10mg·kg-1和 2 0mg·kg-1则Fas和FasL的表达明显低于不给药的缺血再灌流对照组 ,并呈剂量依赖性。结论 脑缺血再灌流可诱导促凋亡基因Fas和FasL在缺血易感部位表达 。

AIM To explore the expression of Fas and FasL genes after ischemia reperfusion in rats and the effect of flunarizine. METHODS Ischemia was induced by four vessel occlusion for 30 min following reperfusion in rats. The biopsy tissues from brain were immunohistochemically assayed with Fas and FasL genes polyclonal antibody. RESULTS The expression of Fas was increased as early as 6 h after the onset of reperfusion. The peak of the expression of Fas occurred 24～48 h after ischemia reperfusion. The expression of FasL was observed 12 h after ischemia reperfusion and peaked at 48～72 h. The expression of Fas and FasL gene was quite obvious in the cortex and hippocampus CA 1, the more sensitive areas to ischemic injury. Flunarizine ip 10 mg·kg -1 and 20 mg·kg -1 obviously inhibited the expression of Fas and FasL in dose dependent manner. CONCLUSION Expression of Fas and FasL in cerebral cortex and hippocampus can be induced by global ischemia reperfusion. Flunarizine significantly inhibited the expression of Fas and FasL genes following ischemia reperfusion.