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目的研究急性一氧化碳中毒(ACOP)后脑海马细胞凋亡和bcl-2、Bax、caspase-3蛋白表达的变化。方法雄性昆明小鼠56只随机分为7组(对照组、ACOP后1h,6h,12h,24h,3d,7d组),每组8只,对照组暴露于空气中,中毒组暴露于一氧化碳(CO)气体中,于相应时间点断头取脑。采用TUNEL、免疫组化法和流式细胞仪观察ACOP后细胞凋亡和caspase-3、bcl-2、Bax蛋白表达的变化。结果ACOP后3d小鼠脑海马凋亡细胞明显增加(P<0.05),第7天达最高(P<0.01);caspase-3蛋白在ACOP后1h表达增加,第3天达到高峰,第7天降至正常;bcl-2蛋白在中毒后1h海马区表达增多,24h达到高峰,第7天大致正常;Bax蛋白在CO中毒1h表达增多,24h达高峰,第7天大致正常。结论ACOP后小鼠脑海马出现迟发的神经元凋亡及凋亡相关因子表达,细胞凋亡可能参与了ACOP迟发脑病的发病机制。
Objective To study the changes of apoptosis and expression of bcl-2, Bax and caspase-3 proteins in hippocampus of rats after acute carbon monoxide poisoning (ACOP). Methods Fifty-six male Kunming mice were randomly divided into 7 groups (control group, 1h, 6h, 12h, 24h, 3d, 7d after ACOP), with 8 rats in each group. The control group was exposed to air and the poisoning group was exposed to carbon monoxide CO) gas, decapitated brain at the appropriate time point. The changes of apoptosis and expression of caspase-3, bcl-2 and Bax protein after ACOP were observed by TUNEL, immunohistochemistry and flow cytometry. Results The apoptotic cells in hippocampus of ACD mice were significantly increased after 3 days (P <0.05), and reached the peak on the 7th day (P <0.01). The expression of caspase-3 protein increased 1 h after ACOP and peaked on the 3rd day. Bcl-2 protein increased in hippocampus 1 h after poisoning, peaked at 24 h, and almost normal on day 7. The expression of Bax protein increased at 1 h CO poisoning, reached the peak at 24 h, and was almost normal on day 7. Conclusion The delayed neuronal apoptosis and the expression of apoptosis related factors appear in hippocampus of ACOP mice. Apoptosis may be involved in the pathogenesis of ACOP delayed encephalopathy.