刘颖菊, 薛春生, 周歧新. 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J. 药学学报, 2000, 35(11): 810-813.
引用本文: 刘颖菊, 薛春生, 周歧新. 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J. 药学学报, 2000, 35(11): 810-813.
LIU Ying-ju, XUE Chun-sheng, ZHOU Qi-xin. EXPRESSION OF FAS AND FASL GENES IN BRAIN AND EFFECT OF FLUNARIZINE ON THESE EXPRESSIONS IN RATS FTER GLOBAL ISCHEMIA-REPERFUSIONJ. Acta Pharmaceutica Sinica, 2000, 35(11): 810-813.
Citation: LIU Ying-ju, XUE Chun-sheng, ZHOU Qi-xin. EXPRESSION OF FAS AND FASL GENES IN BRAIN AND EFFECT OF FLUNARIZINE ON THESE EXPRESSIONS IN RATS FTER GLOBAL ISCHEMIA-REPERFUSIONJ. Acta Pharmaceutica Sinica, 2000, 35(11): 810-813.

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 FTER GLOBAL ISCHEMIA-REPERFUSION

  • 摘要: 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30 min再灌流模型和免疫组织化学染色法。结果 脑缺血再灌流6 h在皮质及海马区即出现Fas表达阳性细胞,24~48 h时达高峰;FasL则在12 h后出现,48~72 h时达到高峰。ip氟桂嗪10 mg.kg-1和20 mg.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,钙拮抗剂氟桂嗪可抑制其表达。

     

    Abstract: 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 CA1, 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.

     

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