论文部分内容阅读
目的:研究依达拉奉对海人酸诱导大鼠癫痫引起神经元损伤的保护作用及其分子机制。方法:SD大鼠随机分为癫痫对照组(saline组)、癫痫组(KA组)和药物对照组(KA+saline组)及依达拉奉组(KA+Ed组)。采用脑室注射海人酸制作大鼠癫痫模型。取海马组织应用Western-blot法检测cleaved caspase-3、FasL和Fas的表达,以免疫共沉淀法检测FasL与Fas的结合;焦油紫染色来观察海马CA1区CA3/DG区锥体细胞形态并计数成活的细胞。结果:癫痫组和药物对照组FasL的表达及其与Fas的结合以及cleaved caspase-3的表达较癫痫对照组显著增加(P<0.05),而依达拉奉组较药物对照组显著降低(P<0.05),Fas的蛋白表达各组间差异未见显著性(P>0.05);依达拉奉明显改善海人酸诱导损伤的神经细胞形态,减少CA1区CA3区神经元的缺失(P<0.05)。结论:依达拉奉可以通过抑制KA诱导FasL的表达及其与Fas的结合,抑制Fas/FasL通路,进而抑制caspase-3的活化对神经细胞发挥保护作用。
Objective: To investigate the protective effect of edaravone on the neuronal damage induced by kainate acid induced epilepsy in rats and its molecular mechanism. Methods: SD rats were randomly divided into epilepsy control group (saline group), epilepsy group (KA group) and drug control group (KA + saline group) and edaravone group (KA + Ed group). Rat intracerebral injection of kainic acid rat epilepsy model. The expression of cleaved caspase-3, FasL and Fas was detected by Western-blot in hippocampus, and the FasL-Fas binding was detected by co-immunoprecipitation. The pyramidal cell morphology of hippocampal CA1 / Living cells. Results: The expression of FasL and its association with Fas and the expression of cleaved caspase-3 in epilepsy group and drug control group were significantly higher than those in epilepsy control group (P <0.05), while those in edaravone group were significantly lower than those in control group (P (P <0.05). No significant difference was observed in the expression of Fas protein between groups (P> 0.05). Edaravone significantly improved neuronal morphology induced by kainate acid and decreased the number of neurons in CA3 area of CA1 (P < 0.05). Conclusion: Edaravone can protect nerve cells by inhibiting the expression of FasL, binding to Fas, inhibiting the Fas / FasL pathway and inhibiting the activation of caspase-3.