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目的短时氧惊厥是否会引起脑海马神经元的凋亡以及神经元在形态上的变化,为氧惊厥的防治提供理论依据积累资料。方法8只实验动物用健康雄性沙土鼠经观察和检疫1周后进行实验。按照体质量采用随机数字法随机分为两组(正常对照组、短时氧惊厥组),每组4只。沙土鼠暴露在0.5MPa压力的高压氧下,引起短时氧惊厥(首次惊厥5min后,减压出舱)后应用HE、TUNEL和免疫组化LSAB染色法观察脑海马神经元形态学变化情况。结果沙土鼠在发生短时氧惊厥后3d,在用HE和TUNEL染色的脑片上未发现海马区神经元的死亡,神经元形态及数目犤(203±14)/mm2犦与对照组犤(200±13)/mm2犦均无明显变化(P>0.5),用免疫组化法染色的脑切片上发现氧惊厥组海马神经元有B细胞淋巴瘤-2基因(bcl-2)蛋白强阳性表达,而对照组则无表达。结论短时氧惊厥未引起脑海马神经元的死亡,但可诱导海马神经元bcl-2基因的蛋白表达,从而提示在一定程度上保护了海马神经元,这可视为海马神经元抗氧惊厥损伤的细胞内保护性机制的反应。
Objective Whether short-term oxygenated convulsions can cause neuronal apoptosis in hippocampus and morphological changes of neurons provide a theoretical basis for the prevention and treatment of oxygen convulsions and accumulate data. Methods Eight experimental animals were tested with healthy male gerbils for one week after observation and quarantine. According to the body weight, random numbers were randomly divided into two groups (normal control group, short-term oxygenated convulsion group), 4 in each group. Gerbils exposed to 0.5MPa pressure of hyperbaric oxygen, causing short-term oxygen convulsion (after the first convulsion 5min, decompression out of space), HE, TUNEL and immunohistochemical LSAB staining was used to observe morphological changes of hippocampal neurons. Results No neuron death was observed in hippocampus of HE and TUNEL brain slices. The morphology and number of neurons (± (203 ± 14) / mm2 3d and control group 犤 (200 ± 13) / mm2 犦 (P> 0.5). Immunohistochemical staining showed that the hippocampal neurons in the oxygenated group had strong positive expression of Bcl-2 gene , While the control group did not express. Conclusions Short-term oxygenated convulsion does not cause death of hippocampal neurons, but can induce the expression of bcl-2 gene in hippocampal neurons, which suggests that hippocampal neurons can be protected to a certain extent. This may be considered as the anticonvulsant in hippocampal neurons Reactions of damaged intracellular protective mechanisms.