摘要
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。
Aim To explore whether transient oxygen convulsion can cause apoptosis and morphlogical changes of neurons in hippocampus and provide theoretical basis for prevention and treatment of oxygen convulsion.Methods 8 healthy male gerbils were used and experiments were carried out after 1 week of observation and quarantine.Gerbils were divided by random number table into normal control and transient convulsion groups with 4 gerbils in each groups.Transient oxygen convulsion was induced by 0.5 MPa hyperbaric oxygen(gerbils were taken out 5 min later following first convulsion),then morphological changes of neurons in hippocampus were observed by HE,TUNEL and immunohistochemical LSAB staining.Results At 3 days after transient convulsion,no apoptosis of neurons was found in brain sections by HE and TUNEL staining,morphology and number of neurons (203± 14)/mm2 showed no obvious changes compared with control group (200± 13)/mm2,(P >0.5).Strong positive expression of B lymphoma 2 gene(bcl 2) protein was found in brain sections stained immunochemically while no expression in control group.Conclusion Transient oxygen doesn't cause neuronal death of neurons in hippocampus,but can induce expression of bcl 2 gene and protect neurons in some degree which might be the intracellular antioxygen convulsion mechanism in hippocampus neurons.
出处
《中国临床康复》
CSCD
2003年第19期2670-2671,共2页
Chinese Journal of Clinical Rehabilitation
基金
解放军总后勤部卫生部课题基金资助(96L003)~~