首页|期刊导航|海南医学院学报|MicroRNA-23a在自身免疫性肺气肿模型大鼠肺泡隔细胞凋亡中的作用

MicroRNA-23a在自身免疫性肺气肿模型大鼠肺泡隔细胞凋亡中的作用OA北大核心CSTPCD

The role of MicroRNA-23a in apoptosis of alveolar septal cells in rats with autoimmune emphysema

中文摘要英文摘要

目的:研究微小RNA-23a(microRNA-23a,miRNA-23a)对自身免疫性肺气肿模型大鼠肺泡隔细胞凋亡的影响.方法:随机将24只雄性SD大鼠分为肺气肿组、正常对照组和miRNA-23a 模拟物(miRNA-23a agomir)干预组.肺气肿组经腹腔注射人脐静脉内皮细胞与完全弗氏佐剂的混合物造模+同miRNA-23a agomir干预组同日尾静脉注射同体积生理盐水;miRNA-23a agomir干预组:同日同肺气肿组方法造模+造模后第1、7、14、21天分别经尾静脉注射miRNA-23a agomir(25 μmol/L);正常对照组同日腹腔注射同剂量完全弗氏佐剂+同miRNA-23a agomir干预组同日经尾静脉注射同体积生理盐水.造模21 d后,取各组大鼠右下肺行苏木精-伊红染色,观察病理学变化,测量平均肺泡数(mean alveolar number,MAN)和平均内衬间隔(mean linear interce-pt,MLI)右上肺经实时定量聚合酶链反应检测miRNA-23a表达水平,通过脱氧核糖核酸末端转移酶介导的缺口末端标记法检测凋亡肺泡隔细胞并计算凋亡指数(Apoptotic index,AI).血清检测抗血管内皮细胞抗体(Antiendothelial Cell Antibodies,AECA)的浓度.结果:(1)各组肺气肿病理改变程度:正常对照组<miRNA-23a agomir干预组<肺气肿组;(2)各组MAN比较:正常对照组>miRNA-23a agomir干预组>肺气肿组,各组差异有统计学意义(P<0.01).各组MLI比较:正常对照组<miRNA-23a agomir干预组<肺气肿组,各组差异均有统计学意义(P<0.01).(3)各组AECA浓度比较:正常对照组<miRNA-23a agomir干预组<肺气肿组,各组差异均有统计学意义(P<0.01).(4)各组miRNA-23a定量表达比较:正常对照组>miRNA-23a agomir干预组>肺气肿组,各组差异有统计学意义(P<0.01).(5)各组肺泡隔AI比较:正常对照组<miRNA-23a agomir干预组<肺气肿组,各组差异均有统计学意义(P<0.01).结论:miRNA-23a表达水平下调可能参与了肺气肿模型大鼠肺泡隔细胞的凋亡,miRNA-23a agomir可减少肺气肿中的肺泡隔细胞凋亡,从而延缓自身免疫性肺气肿疾病进展.

Objective:To investigate the effect of microRNA-23a(miRNA-23a)on the apoptosis of alveolar septal cells in rats with autoimmune emphysema.Methods:Twenty-four male SD rats were randomly divided into the emphysema group,nor-mal control group and miRNA-23a agomir intervention group.The emphysema group was treated with intrabitoneal injection of hu-man umbilical vein endothelial cells and complete Fredrin adjuvant+the same volume of normal saline was injected into the tail vein on the same day as the miRNA-23a agomir intervention group;for miRNA-23a agomir intervention group,on the same day as the emphysema group,+miRNA-23a agomir(25 μM)was injected through the tail vein at 1,7,14 and 21 days after the model-ing,respectively;The normal control group was intraperitoneally injected with the same dose of complete Freund's adjuvant+the same volume of normal saline was injected through the tail vein on the same day.21 days after modeling,hematoxylin-eosin staining was performed on the right lower lung of all rats and pathological changes were observed,mean alveolar number(MAN)and mean linear interce-pt(MLI)were measured.The expression level of miRNA-23a was detected by Quantitative real-time polymerase chain reaction in the right upper lung.Terminal deoxynucleotidyl transferaseme-diated dUTP nick end labeling method detected apoptotic alveolar septal cells and calculated apoptotic index(AI).Serum concentrations of antiendothelial cell antibodies(AECA)were detected.Results:(1)The pathological changes of pulmonary emphysema in the three groups were as follows:normal control group<miRNA-23a agomir intervention group<emphysema group;(2)Comparison of MAN and MLI among the three groups:MAN comparison:normal control group>miRNA-23a agomir intervention group>emphysema group,with statistical signifi-cance among all groups(all P<0.01).MLI comparison:normal control group<miRNA-23a agomir intervention group<emphy-sema group,with statistical significance among all groups(all P<0.01);(3)Comparison of serum AECA concentration in three groups:normal control group<miRNA-23a agomir intervention group<emphysema group,with statistical significance among all groups(all P<0.01);(4)Comparison of miRNA-23a in lung tissue of three groups of rats:normal control group>miRNA-23a agomir intervention group>emphysema group,with statistical significance among all groups(all P<0.01);(5)Three groups of rat alveolar septal cell apoptosis number comparison:normal control group<miRNA-23a agomir intervention group<emphy-sema group,with statistical significance among all groups(all P<0.01).Conclusion:The down-regulated expression of miRNA-23a was involved in the apoptosis of alveolar septal cells in emphysema model rats.miRNA-23a agomir can reduce the apoptosis of alveolar septal cells in emphysema model rats,thereby delaying the progression of autoimmune emphysema disease.

程贵容;卢江桃;张程

遵义医科大学,贵州 遵义 563000贵州医科大学,贵州 贵阳 550001贵州省人民医院,贵州 贵阳 550002||国家卫生健康委员会肺脏免疫性疾病重点实验室,贵州 贵阳 550000

临床医学

自身免疫性肺气肿miRNA-23a肺泡隔细胞凋亡

Autoimmune emphysemamiRNA-23aAlveolar septal cell apoptosis

《海南医学院学报》 2024 (023)

1769-1775 / 7

This study was supported by the Guizhou Science and Technology Plan Project[Guizhou Science and Technology Foundation-ZK(2021)General 350] 贵州省科技计划项目[黔科合基础-ZK(2021)一般 350]

10.13210/j.cnki.jhmu.20240708.003

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