Apaf-1、Mfn2、Caspase-10在慢性阻塞性肺疾病小鼠模型肺组织中的表达

发布时间：2018-10-24 12:03

【摘要】：目的观察小鼠慢性阻塞性肺疾病(COPD)动物模型肺组织中的凋亡蛋白:凋亡蛋白酶活化因子-1(Apaf-1)、线粒体融合蛋白2(Mfn2)、半胱氨酸蛋白酶-10(Caspase-10)的表达,探讨COPD细胞凋亡的机制。方法健康SPF级、6周龄C57BL/6J雄性小鼠30只,适应性饲养2周后,按照随机数字表法分为两组:COPD组采用自制香烟烟雾暴露箱行香烟(含尼古丁0.9 mg,焦油12 mg)烟雾暴露;健康对照组放入另一相同的烟雾发生器中,不燃烧香烟,自由呼吸新鲜空气,自由饮食饮水。两组小鼠均于第91天处死。取肺组织行常规石蜡包埋,运用HE染色、电镜对肺组织形态学进行观察;用免疫组化检测两组小鼠肺组织Apaf-1、Mfn2、Caspase-10蛋白表达水平;用原位检测法测定两组小鼠肺组织内细胞凋亡率。结果 COPD组小鼠形态学结果符合COPD临床病理形态学改变,肺功能提示存在气流受限;COPD组凋亡蛋白Apaf-1、Mfn2、Caspase-10均较健康对照组升高,差异有统计学意义(P0.05);COPD组肺组织内皮细胞凋亡率较健康对照组升高,差异有统计学意义(P0.05)。结论凋亡蛋白Apaf-1、Mfn2、Caspase-10可能通过多种凋亡途径共同促进了COPD细胞凋亡的发生。
[Abstract]:Objective to investigate the expression of apoptotic proteins including apoptotic protease activator 1 (Apaf-1), mitochondrial fusion protein 2 (Mfn2) and cysteine protease 10 (Caspase-10) in the lung tissue of (COPD) model mice with chronic obstructive pulmonary disease (COPD), and to explore the mechanism of COPD cell apoptosis. Methods 30 healthy C57BL/6J male mice of SPF grade and 6 weeks of age were randomly divided into two groups according to the method of random number table after adaptive feeding for 2 weeks. In the COPD group, cigarette smoke exposure (12 mg) containing nicotine 0.9 mg, tar was carried out in a self-made cigarette smoke exposure box. The healthy control group was placed in the same smoke generator, without burning cigarettes, free to breathe fresh air, and to drink freely. The mice in both groups were killed on the 91 th day. The lung tissue was embedded with conventional paraffin wax, the lung tissue morphology was observed by HE staining, the expression of Apaf-1,Mfn2,Caspase-10 protein in lung tissue was detected by immunohistochemistry, and the apoptosis rate in lung tissue was measured by in situ detection. Results the morphologic results of COPD group were consistent with the clinical and pathological changes of COPD, the pulmonary function indicated that there was airflow limitation, and the apoptotic protein Apaf-1,Mfn2,Caspase-10 in COPD group was higher than that in healthy control group. The difference was statistically significant (P0.05). The apoptosis rate of lung endothelial cells in); COPD group was higher than that in healthy control group (P0.05). Conclusion the apoptotic protein Apaf-1,Mfn2,Caspase-10 may promote the apoptosis of COPD cells through multiple apoptotic pathways.
【作者单位】：广东省深圳市龙岗中心医院呼吸内科;遵义医学院珠海校区;
【基金】：广东省深圳市龙岗区科技计划医疗卫生项目(编号:YS2013116)
【分类号】：R563.9;R-332

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