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目的 研究亚硒酸钠对沙土鼠脑缺血再灌注损伤的保护作用及其机制。方法 将 5 0只沙土鼠随机分为 5组 ,Ⅰ组 :假手术组 ;Ⅱ组 :缺血再灌注 1天处死组 ;Ⅲ组 :缺血再灌注 4天处死组 ;Ⅳ组 :硒处理、缺血再灌注 1天处死组 ;Ⅴ组 :硒处理、缺血再灌注 4天处死组。采用夹闭双侧颈动脉法制备沙土鼠脑缺血再灌注模型 ,焦油紫染色 ,光镜下观察各组海马CA1区神经细胞的形态变化 ,TUNEL染色观察神经细胞凋亡情况 ,计算凋亡密度。同时测定脑组织中丙二醛 (MDA)、谷胱甘肽过氧化酶 (GSH PX)的含量。结果 硒处理组沙土鼠缺血再灌注后 ,光镜下病理形态损伤较轻 ,凋亡密度较小 ,GSH PX含量较高。结论 硒对沙土鼠脑缺血再灌注损伤具有保护作用 ,其机制可能与增强脑缺血再灌注早期脑组织中GSH PX的活性 ,抑制氧自由基损伤 ,减轻脂质过氧化反应 ,而减轻缺血再灌注后细胞的坏死和凋亡有关。
Objective To study the protective effect and its mechanism of sodium selenite on gerbil cerebral ischemia-reperfusion injury. Methods Fifty gerbils were randomly divided into five groups: group Ⅰ: sham-operation group, group Ⅱ: ischemia-reperfusion 1-day sacrifice group, group Ⅲ: ischemia-reperfusion 4-day sacrifice group, One day after ischemia-reperfusion, the rats were sacrificed. GroupⅤ: selenium, ischemia-reperfusion 4 days. The model of gerbil cerebral ischemia-reperfusion was established by occlusion of bilateral carotid artery. The morphological changes of hippocampal CA1 neurons in each group were observed under light purple staining and TUNEL staining. The apoptosis density . At the same time, the content of malondialdehyde (MDA) and glutathione peroxidase (GSH PX) in brain tissue were determined. Results After gerbil ischemia-reperfusion in selenium-treated group, the damage of pathological morphology under light microscopy was slight, the apoptotic density was smaller and the content of GSH PX was higher. Conclusion Selenium has a protective effect on cerebral ischemia-reperfusion injury in gerbils. The mechanism may be related to the enhancement of GSH-PX activity in brain tissue during early stage of cerebral ischemia-reperfusion, inhibiting the injury of oxygen free radical, reducing lipid peroxidation, Cell necrosis and apoptosis after blood reperfusion.