中文摘要：

目的：不同浓度脂多糖（LPS）干预哮喘大鼠，探讨其对气道炎症，气道重塑及Toll样受体4（TLR4）mRNA表达水平的影响。方法：SPF级sD大鼠24只随机分为4组（n=6）：正常对照组、低浓度LPS组、高浓度LPS组、哮喘组。以卵清蛋白（OVA）致敏与激发建立大鼠哮喘模型。HE染色观察肺组织病理改变；气道壁嗜酸性粒细胞（EOS）计数观察炎症细胞浸润情况；测定气道阻力；图像分析软件测定气道壁厚度；RT-PCR方法检测大鼠气道平滑肌TLR4mRNA表达水平。结果：哮喘组、低浓度LPS组及高浓度LPS组气道阻力、气道壁EOS计数及气道壁厚度均较正常对照组显著增加（P〈0．01），其中高浓度LPS组上述指标较哮喘组及低浓度LPS组均显著降低（P〈0．05）；低浓度LPS组、高浓度LPS组大鼠气道平滑肌TLR4mRNA表达水平均显著高于哮喘组（P〈0．01），其中高浓度LPS组表达水平亦明显高于低浓度LPS组（P〈0．05）。结论：TLR4在哮喘气道炎症及气道重塑中起重要作用，LPS通过激活TLR4在哮喘气道炎症及气道重塑的发病过程中可能发挥双向调控作用。

英文摘要：

Objective： To investigate the effects of lipopolysaccharide（LPS） on airway inflammation, airway remodeling and the expression of ToU-like receptor 4 （TLR4） mRNA in asthmatic rats. Methods： Twenty-four SPF level SD rats were randomly divided into four groups （ n = 6） ：control group,low dose of LPS group,high dose of LPS group and asthma group. Using ovalbumin（OVA） to sensitize and challenge to establish asthmatic rat model. Observed pathological changes of lung tissue by HE staining, inflammatory cell infiltration was observed by airway wall eosinophils（EOS） counts; airway resistance was determined; image analysis software was used to detemaine the thickness of airway wall, detected airway smooth muscle TLR4 expression levels by RT-PCR. Results： The rat airway resistance and the EOS number of airway wall and the thickness of airway wall in asthma group, low dose of LPS group and high dose of LPS group were significantly higher than those in control group（ P 〈 0.01）. The above-mentianed pmmneters of high dose of LPS group showed significantly lower than those in asthma group and low dose of LPS group（ P 〈 0.05）. The expression of rat airway smooth muscle TLR4 mRNA in low dose of LPS group and high dose of LPS group were significantly higher than those in asthma group（ P 〈 0.01 ）. And the expression of rat airway smooth muscle TLR4 mRNA in high dose of LPS group was significantly higher than that in low dose of LPS group（ P 〈 0.05）. Condusion： TLR4 plays an important role in asthmatic airway inflammation and airway remodeling, LPS may play double-sided regulation in asthmatic airway inflammation and airway remodeling by activated TLR4.