依达拉奉对一氧化碳中毒迟发性脑病小鼠脑细胞凋亡及相关基因表达的影响

Effect of edaravone on poisoning delayed cerebral cell apoptosis and related gene expression in mouse encephalopathy of carbon monoxide

关键词:  一氧化碳  依达拉奉  迟发性脑病  细胞凋亡  中毒  小鼠

Key words:  [Key words] 　carbon monoxide  edaravone  delayed encephalopathy  apoptosis  poisoning  mice

摘要:

目的　观察自由基清除剂依达拉奉对CO中毒迟发性脑病(DNS)小鼠细胞凋亡及相关基因表达的影响。方法　雄性昆明小鼠72只，18～22 g，随机分为对照组、中毒组、生理盐水组和依达拉奉组,一氧化碳腹腔注射建立一氧化碳中毒迟发性脑病的模型。染毒后5～21 d生理盐水组腹腔注射生理盐水，依达拉奉组腹腔注射依达拉奉，治疗结束后处死动物每组用免疫组化检测脑组织神经细胞的Bcl-2、Bax蛋白表达。应用流式细胞仪法检测脑凋亡细胞。 结果　与中毒组（38.5±0.58）及生理盐水组（36.5±0.46）比较，依达拉奉组（24.5±0.48）神经细胞凋亡显著减少(P<0.05)；凋亡调控基因Bax／Bcl-2值明显降低(P<0.05)。结论　依达拉奉注射液对CO中毒迟发性脑病的脑保护作用机制可能与干预脑细胞凋亡相关基因表达并减少神经细胞凋亡有关。

Abstract:

[Abstract] Objective　To observe the effect of radical scavenger edaravone on apoptosis and related genes of CO induced delayed encephalopathy in mice. Methods　72 male Kunming mice, 18-22 g, were randomly divided into control group, poisoning group, saline group and edaravone group. Establishment of carbon monoxide poisoning delayed encephalopathy model by intraperitoneal injection of carbon monoxide.Saline group were injected with saline. Edaravone group were injected edaravone after exposure for 5-21 d. Immunohistochemistry was used to observe bcl-2 and bax protein expressions, and flow cytometry was used to detect cell apoptosis to nerve cells of the brain. Results　Compared with poisoning group (38.5±0.58) and saline group (36.5±0.46), edaravone group (24.5±0.48) significantly reduced in the number of apoptotic neuronal cells (P<0.05) and significantly decreased in Bax/Bcl-2 value (P<0.05). Conclusion　Edaravone might have protection effect on brain with carbon monoxide poisoning delayed encephalopathy through decreasing apoptosis of nerve cells.