一氧化碳中毒迟发性脑病小鼠脑HO-1表达变化及其与细胞凋亡的关系

发布时间：2018-03-06 15:52

本文选题：一氧化碳中毒　切入点：血红素加氧酶-　出处：《中国临床解剖学杂志》2014年06期 　论文类型：期刊论文

【摘要】：目的研究一氧化碳(carbon monoxide,CO)中毒后不同时间点小鼠脑内血红素加氧酶-1(heme oxygenase-1 HO-1)的表达变化;检测CO中毒后不同时间点小鼠脑内神经细胞凋亡及相关基因表达的情况。探讨血红素氧化酶-1与脑细胞凋亡之间的变化关系。方法使用腹腔注射CO的方法制备CO中毒迟发性脑病(Delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)的模型,应用Western blotting法观察HO-1蛋白水平的表达,应用流式细胞仪法检测凋亡细胞,采用SABC免疫组化法观察Bcl-2、Bax在蛋白水平的表达。结果 Western blotting法HO-1蛋白表达情况:空气对照组表达较少,CO中毒组1 d表达增加(1.14±0.43,P0.01),3 d达高峰(2.91±1.07,P0.01),21 d仍高于对照组(P0.01)。细胞凋亡情况:空气对照组各时间点细胞凋亡百分数较少,CO中毒组12 h凋亡细胞百分数数增加(21.95±24,P0.01),5 d达高峰(34.27±4.19,P0.01),21 d时(9.25±1.16)仍高于对照组。凋亡相关蛋白表达:Bax在中毒后表达增加,3 d达高峰(34.5±0.58,P0.01),Bcl-2在3 d减少至最低(12.5±3.69,P0.01),Bax/Bcl-2的比值于3 d时达最大。结论 CO中毒迟发性脑病小鼠海马区HO-1蛋白表达明显增高,凋亡细胞明显增多且与HO-1的表达变化一致。HO-1表达增高可能参与了CO中毒所致脑损伤的发病机制。
[Abstract]:Objective to study the changes of heme oxygenase-1heme oxygenase-1 (HO-1) expression at different time points after carbon monoxide carbon monoxide (CO) poisoning in mice. To investigate the relationship between the changes of heme oxygenase-1 and the apoptosis of brain cells in mice at different time points after CO poisoning. Methods CO was prepared by intraperitoneal injection of CO. Model of delayed encephalopathy after acute carbon monoxide poisoning DEACMP. Western blotting assay was used to detect the expression of HO-1 protein, and flow cytometry was used to detect the apoptotic cells. Results the expression of HO-1 protein by Western blotting method was observed by SABC immunohistochemical method. Results the expression of HO-1 protein in the air control group was increased by 1.14 卤0.43P0.01P0.01a on the 1st day, and the expression of HO-1 protein was still higher than that of the control group on the 21st day after reaching the peak of 2.91 卤1.07g / L P0.01a. Results the expression of HO-1 protein in the air control group was still higher than that in the control group (P 0.01). Death: the percentage of apoptotic cells in the air control group at each time point was higher than that in the control group at 12 h after CO poisoning. The apoptotic cell percentage in the air control group was increased by 21.95 卤24p 0.01g / h to a peak of 34.27 卤4.19P0.01g / 21 days after poisoning, and the expression of apoptosis-related protein was still higher than that of the control group. The expression of apoptosis-related protein (VBA x) was increased after poisoning. The ratio of HO-1 / Bcl-2 in hippocampus of mice with delayed encephalopathy due to CO poisoning was significantly higher than that of control group at 3 days after 3 days of treatment, and the ratio of Bax-P / Bcl-2 was reduced to a minimum of 12.5 卤3.69. Conclusion the expression of HO-1 protein in hippocampus of mice with delayed encephalopathy induced by CO poisoning was significantly increased. The increase of apoptotic cells was consistent with the expression of HO-1. The increased expression of HO-1 may be involved in the pathogenesis of brain injury induced by CO poisoning.
【作者单位】：大连医科大学附属第二医院重症医学科;大连市中心医院神经内科;
【基金】：大连医科大学附属第二医院2009年青年科研基金课题资助
【分类号】：R749.63

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