中文摘要：

目的：探讨Toll样受体4（TLR4）在哮喘状态下气道平滑肌细胞（ASMCs）增殖、凋亡中的作用。方法：建立哮喘大鼠模型，分离、培养哮喘大鼠气道平滑肌细胞，应用小分子RNA干扰技术、脂质体转染法进行小分子RNA-TLR4的转染、MTT法检测细胞增殖、TUNNEL法检测细胞凋亡情况、逆转录聚合酶链式反应（RT-PCR）和Western blot检测细胞中TLR4的mRNA和蛋白的表达水平。结果：TNF-α组ASMCs增殖反应显著高于对照组、siRNA-TLR4转染组、TNF-α＋siRNA-TLR4转染组，而siRNA-TLR4转染组的ASMCs增殖反应显著低于对照组；siRNA-TLR4转染组和TNF-α＋siRNA-TLR4转染组细胞凋亡率显著高于对照组，而TNF-α组ASMCs的凋亡率显著低于对照组、siRNA-TLR4转染组、TNF-α＋siRNA-TLR4转染组；对照组和TNF-α组TLR4的mRNA和蛋白表达水平显著高于siRNA-TLR4转染组、TNF-α＋siRNA-TLR4转染组，而TNF-α组TLR4的mRNA和蛋白表达水平显著高于对照组。结论：TLR4的激活可能促进哮喘气道平滑肌细胞的增殖，抑制凋亡，从而在哮喘气道重构中起重要作用。

英文摘要：

Objective： To explore the role of Toll like receptor 4（TLR4） in the asthmatic rat airway smooth muscle cell （ASMCs） prolifelation and apoptosis. Methods： Established rat model of asthma,isolated and cultured rat ASMCs in asthma,using methods of small molecule RNA interference technology and lipofecfion method, for small molecule RNA-TLR4 transfection, detected proliferation of ASMCs by MTT minim colorimetry, apoptosis of ASMCs by TUNNEL, the expression of TLR4 protein and mRNA were detected by Western blot and RT-PCR in cells. Results： The proliferation of ASMCs in TNF-α group were signiticanfly higher than that in control group and siRNA-TLR4 transfection group and TNF-α ＋ siRNA-TLR4 transfection group respectively and the proliferation of ASMCs in siRNA-TLR4 transfction group was lower than that in control group. The apoptosis rate of ASMCs in TNF-α group was lower than that in control group, siRNA-TLR4 transfection group and TNF-α ＋ siRNA-TLR4 transfection group respectively and the apoptosis rate of ASMCs in siRNA-TLR4 transfection group and TNF-α ＋ siRNA-TLR4 transfection group were significantly higher than those in control group. The rnRNA and protein expression of TLR4 in control group and TNF-α group were significantly higher than those in siRNA-TLR4 transfection group and TNF-α ＋ siRNA-TLR4 transfection group. The mRNA and protein expression of TLR4 in TNF-α group were significantly higher than those in control group（ P 〈0.01）. Conclusion： Activation of TLR4 may contribute to asthmatic airway smooth muscle cell proliferation, inhibiting apoptosis and play an important role in airway remodeling in asthma.