一氧化碳中毒迟发性脑病模型小鼠脑内血红素加氧酶1mRNA和蛋白的表达

Expression of heme oxygenase-1 mRNA and protein after delayed encephalopathy in carbon monoxide poisoning mice

背景:研究表明一氧化碳中毒迟发性脑病症状的出现与一氧化碳中毒后神经组织细胞凋亡持续发生关系较大。有关血红素加氧酶的细胞保护作用尤其在脑损伤中的细胞保护作用还存在争议。目的:观察一氧化碳中毒后不同时间点小鼠脑内血红素加氧酶1 mRNA和蛋白的表达变化。方法:雄性昆明小鼠随机分为2组,一氧化碳中毒组腹腔注射一氧化碳制备一氧化碳中毒迟发性脑病模型,空气对照组腹腔注射空气。应用原位杂交及Western blot法观察两组在不同时间点海马区血红素加氧酶1mRNA及蛋白表达变化。结果与结论:空气对照组血红素加氧酶1 mRNA表达阳性细胞较少,染色较浅;一氧化碳中毒组海马阳性细胞数较多,染色较深。血红素加氧酶1 mRNA在1 d表达增加(P<0.01),3 d达高峰(P<0.01),5 d时下降(P<0.01),21 d时仍高于空气对照组(P<0.01)。血红素加氧酶1蛋白表达与血红素加氧酶1 mRNA表达变化相一致。结果表明血红素加氧酶1 mRNA及其蛋白的表达增加可能在一氧化碳中毒所致迟发性脑病的发病机制中起重要作用。

BACKGROUND：Currently delayed encephalopathy is closely related with the cel apoptosis in nerve tissue after carbon monoxide （CO） poisoning. The protective effect of heme oxygenase-1, especial y in the brain injury remains controversial. OBJECTIVE：To observe heme oxygenase-1 mRNA and protein expression at different time points after CO poisoning in the mouse brain. METHODS：Male Kunming mice, weighing 18-22 g, were randomly divided into CO poisoning group and air control group. The model of delayed encephalopathy after acute CO poisoning was established with intraperitoneal injection of CO. Air control group was intraperitoneal y injected with air. In situ hybridization and western blot analysis were applied to observe the heme oxygenase-1 mRNA and protein expression in the hippocampus of mice in the two groups at different time points. RESULTS AND CONCLUSION：There were few positive cel s for heme oxygenase-1 mRNA expression in the air control group, with light staining;but a large number of positive cel s for heme oxygenase-1 mRNA expression in CO poisoning group, with deep staining. The heme oxygenase-1 mRNA expression was increased at 1 days （P〈0.01）, reached a peak at 3 days （P〈0.01）, decreased at 5 days （P〈0.01）, and stil higher than air control group at 21 days （P〈0.01）. Changes of heme oxygenase-1 protein expression were consistent with heme oxygenase-1 mRNA expression. The upregulated expression of heme oxygenase-1 mRNA and protein plays a crucial role in the pathogenesis of delayed encephalopathy after CO poisoning.