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目的探讨亚硒酸钠对沙土鼠脑缺血/再灌注(I/R)损伤的保护作用及其机制。方法实验分3组。采用夹闭双侧颈动脉法制备沙土鼠前脑I/R(2,4 d)模型,焦油紫染色,光镜下观察各组海马CA1区神经元的形态变化,电镜下超微结构变化。同时测定脑组织中丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)的含量。结果硒处理组沙土鼠脑I/R后,神经元病理损伤减轻,GSH-PX和SOD含量增多,与对照组比较有显著差异(P<0.01,P<0.05)。MDA含量减少。结论亚硒酸钠对沙土鼠脑I/R损伤具有保护作用,其机制可能和增强脑I/R早期脑组织中抗氧化酶的抗氧化作用有关,可能存在对脑缺血耐受的预处理机制。
Objective To investigate the protective effect of sodium selenite on gerbil brain injury induced by cerebral ischemia / reperfusion (I / R) and its mechanism. Methods The experiment was divided into 3 groups. The occlusion of bilateral carotid arteries was used to prepare the I / R (2,4 d) model of the gerbil forebrain. Tar blue staining and light microscopy were used to observe the morphological changes of hippocampal CA1 neurons and ultrastructural changes under electron microscope. At the same time, the content of malondialdehyde (MDA), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in brain tissue were determined. Results After I / R of selenium-treated group, the pathological damage of neurons was alleviated and the content of GSH-PX and SOD increased. Compared with the control group, there was significant difference (P <0.01, P <0.05). MDA content decreased. Conclusion Sodium selenite has a protective effect on brain I / R injury in gerbils, and its mechanism may be related to enhancing antioxidant activity of antioxidant enzymes in brain I / R early brain tissue. There may be preconditioning for cerebral ischemic tolerance mechanism.