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目的研究Wnt/β-catenin信号通路在哮喘气道炎症和气道重塑中的作用,探讨青蒿琥酯(artesunate,ART)治疗哮喘的可能机制。方法采用卵白蛋白(OVA)激发和雾化吸入的方式建立哮喘模型,并予以药物治疗。观察各组大鼠肺组织的病理形态改变、外周血、支气管肺泡灌洗液(BALF)白细胞计数;Image-Pro plus 6.0图像分析软件测量大鼠肺组织支气管壁厚度和平滑肌厚度;免疫组化法检测大鼠肺组织β-catenin和WISP-1表达情况,RT-PCR检测大鼠肺组织WISP-1表达情况,ELISA法检测血清及BALF中IL-6的表达情况。结果 ART干预哮喘组大鼠气道炎性细胞浸润、支气管壁厚度、平滑肌厚度均明显低于哮喘组大鼠,差异有统计学意义(P<0.01);ART干预哮喘组肺组织β-catenin、WISP-1蛋白和WISP-1 m RNA的表达均明显低于哮喘组,差异有统计学意义(P<0.01);ART干预哮喘组大鼠血清及BALF中IL-6水平表达均明显低于哮喘组,差异有统计学意义(P<0.01)。结论 ART改善哮喘大鼠气道炎症及气道重塑的机制可能与抑制Wnt/β-catenin信号通路活性及下调IL-6水平有关。
Objective To investigate the role of Wnt / β-catenin signaling pathway in airway inflammation and airway remodeling in asthma and to explore the possible mechanism of Artesunate (ART) in the treatment of asthma. Methods The model of asthma was established by ovalbumin (OVA) challenge and nebulized inhalation, and the drug was given to the asthma model. The pathological changes of the lung tissue of the rats in each group were observed, the white blood cell counts of peripheral blood and bronchoalveolar lavage fluid (BALF) were measured, the bronchial wall thickness and smooth muscle thickness were measured by Image-Pro plus 6.0 image analysis software, the immunohistochemistry The expression of β-catenin and WISP-1 in rat lung tissue was detected. The expression of WISP-1 in lung tissue was detected by RT-PCR. The expression of IL-6 in serum and BALF was detected by ELISA. RESULTS: ART intervention in asthmatic rats significantly decreased airway inflammatory cell infiltration, bronchial wall thickness and smooth muscle thickness in asthmatic rats (P <0.01), and the levels of β-catenin, The expression of WISP-1 protein and WISP-1 m RNA in asthma group were significantly lower than those in asthma group (P <0.01). The levels of IL-6 in serum and BALF of ART intervention asthma group were significantly lower than those in asthma group Group, the difference was statistically significant (P <0.01). Conclusion The mechanism of ART on airway inflammation and airway remodeling in asthmatic rats may be related to the inhibition of Wnt / β-catenin signaling pathway and the downregulation of IL-6.