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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 preventive effect of butylphthalide on cortical neurons in cerebral ischemia-reperfusion (IR) rats and its possible mechanism. Methods: The model of right focal cerebral ischemia-reperfusion in rats was made by modified suture method. The expression of Fas / Fas L and the ultrastructure of cortical neurons in ischemia-reperfusion injury were observed by immunohistochemistry and electron microscopy . Results: The expressions of Fas and Fas L positive cells in the sham operation group were normal and the morphology of the neurons was normal. The expression of Fas and Fas L in the model group was significantly increased, the neuron necrosis was more common, the membrane was intermittent or disintegrated, the mitochondria swollen, (P <0.01). Compared with the model group, the positive expression area of Fas and Fas L in the butylphthalide pretreatment group was decreased (P <0.01). Most of the neurons were normal and the nuclear model was relatively intact, Chromatin distribution is more uniform mitochondrial lesion mitigation, endoplasmic reticulum tends to normal, rare apoptotic cells. CONCLUSION: Butylphthalide preconditioning can down-regulate the expression of Fas and Fas Lys in cortical neurons, reduce the ultrastructural damage of ischemia-reperfusion neurons and play a preventive and protective role in IR injury.