摘要
目的:探讨丁苯酞对大鼠脑缺血再灌注(IR)皮质神经元的预防性保护作用及其可能机制。方法:采用改良线栓法制备大鼠右侧脑局灶性缺血再灌注模型;免疫组织化学法和电子显微技术观察缺血再灌注皮质神经元Fas/Fas L的表达和超微结构改变。结果:假手术组偶见Fas、Fas L阳性细胞表达,神经元形态正常;模型组Fas、Fas L阳性表达明显增多,神经元坏死多见,胞膜断续或崩解,线粒体肿胀、嵴断裂,高尔基复合体肿胀扩张,核膜曲折不光滑;与模型组比较,丁苯酞预处理组Fas、Fas L阳性表达面积率降低(P<0.01),多数神经元较正常,核模较完整,染色质分布较均匀,线粒体损伤减轻,内质网趋于正常,凋亡细胞少见。结论:丁苯酞预处理可下调皮质神经元Fas、Fas L阳性表达,减轻缺血再灌注神经元超微结构的损伤,对脑IR损伤有一定的预防性保护作用。
Objective： To investigate the effect of 3-n-butylphthalide（NBP） on the expression of Fas/FasL and ultra- structure induced by focal cerebral ischemia reperfusion（IR） cortex in rats and the mechanism. Methods： The model of focal cerebral ischemia reperfusion was built up on rats using the suture embolic method. The expression of Fas/FasL and ultrastructure in the neurons of cerebral cortex were observed by immunohistochemical techniques and transelectron micro- scope. Results：A few positive cells were positive for Fas/FasL and the ultrastructure was normal in the sham operated group ; in the model group, the positive area rate of Fas/FasL increased, many necrosis were observed, part of membrane dissolved, mitochondria and Golgi complex swelling with endoplasmic reticulum dilatation, nuclear membrane was fold and incomplete. Compared to the model group, in the NBP group, the positive area rate of Fas/FasL decreased sharply, the shape of cells was relatively regular, apoptosis was rare, mitochondria sweUing decreased, endoplasmic reticulum and nuclear membrane tended to normal and complete, chromatin showed relatively uniform. Conclusion ： NBP can protect cerebral cortex IR injury by down regulating the expression of Fas/FasL and improving the ultrastructure of neurons.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2015年第4期493-496,共4页
Chinese Journal of Neuroanatomy
基金
河北省教育厅教育科学计划项目(JYGH2010048)
