【摘要】 目的研究气道平滑肌细胞(ASMCs)增殖过程中TGF-β1分泌释放水平与Th1/Th2细胞分化的特异性细胞因子的关系,并探讨KATP通道开放剂对哮喘气道重塑的作用机制。方法体外构建增殖型ASMCs与淋巴细胞共培养的细胞模型,KATP通道开放剂尼可地尔干预,并设立对照;ELISA法检测上清液中TGF-β1的释放水平;流式细胞表面抗原法检测共培养体系中的Th1/Th2的表达差异。结果 TGF-β1的表达与ASMCs增殖呈正相关,而尼可地尔可下调TGF-β1的表达(P<0.01);增殖型AMSCs促进CD4+T细胞由Th1向Th2分化,Th2优势应答,IL-4表达升高,Th1型细胞因子IFN-γ减少,Th1/Th2平衡失调;尼可地尔可作用Th1细胞百分率升高,而Th2细胞百分率降低(P<0.05)。结论尼可地尔通过抑制ASMCs增殖而调控TGF-β1分泌表达,并可以逆转Th1/Th2免疫失衡。更多还原

【Abstract】 Objective to investigate the relationship of the change of TGF-β1 and the expression cytokines of Th/Th2 in the progress of ASMCs proliferation,and explore the mechanisms of effect of ATP sensitive K+channels opener on airway remodeling of asthma.Methods Co-cultured cell model was treated with ATP sensitive K+channels opener Nicorandil,and established the control groups.The change of TGF-β1 and Th1/Th2 cytokines expression were detected before and after drugs action by ELISA and FCM.Results The serum levels of TGF-β1 had positive correlation with the proliferation of ASMCs.After trade with Nicorandil,the secretin of TGF-β1 was dropped significantly(P < 0.01).The proliferative ASMCs influence the differentiation of CD4+T cells and enhance cytokine synthesis in Th2 cells and a predominance of Th2 cells,which lead a negative regulatory role on the development of Th1 cells.Nicorandil upregulated the percentage of Th1 cells and downregulated the percentage of Th2 cells.Conclusion ATP sensitive K+channels opener Nicorandil may regulate the expression of TGF-β1 by inhibiting the proliferation of ASMCs and rever the immune imbalance of Th1/Th2.更多还原