戊四氮致痫大鼠脑内热休克蛋白70的表达

Induction of heat shock Protein 70 in the rat brain after pentylenetrazole-induced seizures

目的：探讨热休克蛋白70（HSP70）在癫痫大鼠脑内的表达情况及其意义。方法：采用戊四氮致痫模型。应用免疫组织化学及常规清理检查的方法进行研究。结果：在正常大鼠脑内未见HSP70免疫反应（IR）阳性细胞，成四氮致痫12小时后脑内开始出现HSP70IR阳性细胞，24小对IR达高峰．3天后开始下降．7天后消失。HSP70主要在边缘系统（尤其是海马的CA1、CA3、CA4区）、大脑皮质（尤其是颞叶皮质，梨状皮质）等区域表达。同时常规病理检查发现，上述区域散在出现受损的异常神经元。结论：癫痫发作可诱导HSP70在大鼠脑内广泛表达。HSP70表达可作为神经元受损的一个早期指标。

Objective:To investigate the expression of heat shock protein 70(HSP70) in the rat brainafter seizures. Methods:A pentylenetetrazole (PTZ) induced seizure model was used. The expression ofheat shock protein 70 (hsp70) and the extent neuronal damage were studied by immunohistochemistry andhistopathological methods. Results: The hsp70 immumoreacivity (IR) was not detected in the brain ofempty control rats. HSP70IR was observed in thc rats brain at 12h following PTZ injection, at 24h,strong expression was observed. HSP70IR declined there days after PTZ injection and completely disap-peared after seven days. HSP70IR was detected mainly in The cortex (temporal、piriform cortex), and hip-pocampus (CA1、CA3、CA4 sector). Injured neurons werc also found in this region by histopathological ex-amination. Conclusion: HSP70 was induced in the rat brain after PTZ-induced seizure - HSP70 expressionis a valuable carly marker of neuronal injury.