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目的探讨哮喘大鼠发病过程中,肝细胞生长因子(HGF)在其气道内表达的变化及血管紧张素II受体AT1拮抗剂对其表达的影响。方法清洁级SD大鼠48只,随机分为正常对照组、卵蛋白(OVA)激发3 d组、OVA激发2周组、OVA激发4周组、OVA激发4周后使用AT1受体拮抗剂组、OVA激发4周后使用盐水对照组。观察OVA激发的不同时间、药物干预后哮喘大鼠气道的病理改变;免疫组化方法观察HGF、血管紧张素II(AngII)、转化生长因子(TGF)-β1表达的变化。结果HGF在OVA激发3 d即明显高于正常对照组(P<0.05),OVA激发2周HGF在气道中的表达水平最高,OVA激发4周时下降;AngII、TGF-β1表达水平随OVA激发时间的延长而持续上升;使用AT1受体拮抗剂后,气道HGF表达水平有所上升,而AngII、TGF-β1均下降,同时哮喘大鼠的气道重塑有所改善。结论HGF在哮喘发病过程中起保护作用,AngII、TGF-β1对HGF具有负向调节作用,AT1受体拮抗剂在一定程度上可提升内源性HGF表达,改善哮喘大鼠的气道重塑。
Objective To investigate the changes of hepatocyte growth factor (HGF) expression in asthmatic rats and the effect of angiotensin II receptor (AT1) antagonist on its expression. Methods Forty-eight clean SD rats were randomly divided into normal control group, OVA challenge 3 d, OVA challenge 2 weeks, OVA challenge 4 weeks, OVA stimulation 4 weeks, AT1 receptor antagonist Saline control group was used 4 weeks after OVA challenge. The pathological changes of airway in asthmatic rats were observed at different times after OVA challenge. The expressions of HGF, AngII and TGF-β1 were observed by immunohistochemistry. Results The level of HGF in OVA induced 3 days was significantly higher than that in control group (P <0.05). The expression level of HGF in airway was the highest at 2 weeks after OVA challenge, and decreased at 4 weeks after OVA challenge. The expression of Ang II and TGF- Time prolonged and continued to increase; use of AT1 receptor antagonist, airway HGF expression levels increased, while AngII, TGF-β1 decreased, while airway remodeling improved asthma in rats. Conclusions HGF plays a protective role in the pathogenesis of asthma. AngII and TGF-β1 have a negative regulatory effect on HGF. AT1 receptor antagonist may enhance the expression of endogenous HGF to some extent and improve airway remodeling in asthmatic rats .