活化蛋白-1在急性一氧化碳中毒迟发性脑病大鼠海马的表达变化

发布时间：2018-06-07 22:47

本文选题：急性一氧化碳中毒迟发性脑病 + 活化蛋白-　；参考：《中国免疫学杂志》2017年05期

【摘要】：目的:观察急性一氧化碳中毒后不同时间点大鼠海马AP-1的表达变化。方法:腹腔注射一氧化碳的方法制备一氧化碳中毒迟发性脑病模型,HE染色观察大鼠海马区病理变化,免疫组化及Western blot法检测AP-1的表达水平,TUNEL染色计数海马CA1区凋亡神经元。结果:HE染色,空气组(AC组)、空白组(BC组)各时间点海马区细胞形态正常;一氧化碳组(CO组)海马区细胞肿胀、细胞数目减少,排列紊乱,细胞间隙扩大,细胞核碎裂、深染、固缩。免疫组化:CO组各时间点AP-1表达量均高于AC组及BC组,3 d达峰值,组内第3天与其余各时间点比较差异有统计学意义(P0.05)。Western blot:AP-1表达在时间分布趋势上与免疫组化结果一致。TUNEL染色:CO组各时间点凋亡指数均较AC组、BC组多,于毒染后7 d达高峰差异有统计学意义(P0.05)。结论:大鼠海马区AP-1表达增高,可能进一步导致细胞凋亡和炎症免疫反应,成为DEACMP发病的重要机制之一。
[Abstract]:Aim: to observe the changes of AP-1 expression in hippocampus of rats at different time points after acute carbon monoxide poisoning. Methods: the delayed encephalopathy model of carbon monoxide poisoning was made by intraperitoneal injection of carbon monoxide. The pathological changes of hippocampus were observed by HE staining. The expression of AP-1 was detected by immunohistochemistry and Western blot method. The apoptotic neurons in CA1 area of hippocampus were counted by Tunel staining. Results the morphology of hippocampal cells in the air group (AC group) and blank group (BC group) was normal at every time point, and in the carbon monoxide group (CO group) the hippocampal cells were swollen, the number of cells decreased, the number of cells was disordered, the intercellular space was enlarged, the nucleus was broken up and stained deeply. Shrinkage. The expression of AP-1 in the 30% CO group was higher than that in the AC group and BC group at 3 days. On the 3rd day, there was significant difference between the other time points and the other time points. The expression of AP-1 in Western blot: AP-1 was consistent with the immunohistochemical results in time distribution. The apoptotic index was higher in TUNEL + CO group than in AC group. There was significant difference in peak value at 7 days after poisoning (P 0.05). Conclusion: the increased expression of AP-1 in rat hippocampus may further lead to apoptosis and inflammatory immune response, which may be one of the important mechanisms of DEACMP.
【作者单位】：西南医科大学附属医院;
【分类号】：R595.1;R747.9

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