Objective:To investigate the expression change and functions of miR-23b in the airway smooth muscle cells (ASMCs) of asthma mice.Methods:Sixteen female BALB/c mice of clean grade were randomly divided into a normal group and an asthma group.Ovalbu-min (OVA) was used to establish the asthmatic mice model.At 24-48 h after the last irritation,airway smooth muscles were collected and the expression of miR-23b in normal and asthma mice were analyzed via q-PCR.Meanwhile,ASMCs from both normal control group and asthma model group were isolated and cultured by tissue explants adherent method.MiR-23b mimics or mimic NC were transfect into asthma model mice and the AMSCs were collected as well.The proliferation,apoptosis and TGFβR2 expression of the four group ASMCs were detected by CCK8,flow cytometry and western blotting,respectively.Results:Compared with normal mice,the expression of miR-23b was decreased significantly in the airway smooth muscles of asthma mice.Compared with normal control ASMCs,the proliferation of asthma model ASMCs was increased notably (P＜0.05).But after transfected with miR-23b mimics,the proliferation and apoptosis of asthma model ASMCs were decreased compared to asthma model ASMCs.And the expression of TGFβR2 was reduced after transfected with miR-23b mimics (all P＜0.05).Conclusion:The decreased expression of miR-23b might contribute to the over-proliferation of asthma model ASMCs and the decrease of apoptosis,which might be related to the down-regulation of TGFβR2.%目的:观察miR-23b在哮喘小鼠气道平滑肌组织中的表达情况,并探讨miR-23b对体外气道平滑肌细胞(ASMCs)生物学功能的影响及其机制.方法:将16只BALB/c小鼠随机分为哮喘模型组和正常对照组,每组8只.以卵蛋白(OVA)致敏、激发,构建哮喘小鼠模型.在末次激发后24～48 h内取小鼠气道平滑肌组织,荧光定量PCR (q-PCR)法检测两组小鼠气道平滑肌组织中miR-23b的表达.采用组织块贴壁法分离两组小鼠ASMCs并分别将其作为正常对照组和哮喘模型组.对哮喘模型组ASMCs分别转染miR-23b mimics和mimics NC.采用CCK8、流式细胞术和western blotting法分别检测4组ASMCs的增殖、凋亡和细胞转化生长因子受体2 (TGFβR2)蛋白的表达情况.结果:与正常对照组相比,哮喘模型组小鼠气道平滑肌组织中miR-23bmRNA相对表达量明显减少(P＜0.05).哮喘模型组ASMCs增殖速度明显增加(P＜0.05);经miR 23bmimics转染后,与哮喘模型组相比,miR-23b mimics组ASMCs的增殖速度减慢,同时细胞凋亡率升高,TGFpR2蛋白表达量降低,差异均有统计学意义(均P＜0.05).结论:哮喘小鼠气道平滑肌组织中miR-23b表达降低,可导致AMSCs过度增殖,细胞凋亡减少,该作用机制可能与miR 23b下调哮喘小鼠AMSCs中TGFpR2的表达有关.
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