b-FGF和NF-κB在哮喘大鼠肺内的表达及布地奈德干预的作用

目的：探讨哮喘大鼠发病过程中碱性成纤维细胞生长因子(b-FGF)和核因子-κB（NF-κB）在气道内表达的变化，及布地奈德的干预对其表达的影响。方法：清洁级Sprague-Dawley雄性大鼠45只，随机分为对照组、哮喘组、干预组。观察卵蛋白激发及用布地奈德干预后哮喘大鼠气道的病理变化；免疫组织化学染色观察b-FGF和NF-κB蛋白表达的变化。结果：布地奈德干预减轻了哮喘大鼠气道损伤。B-FGF和NF-κB在对照组中呈弱阳性表达，在哮喘组中表达明显增加，使用布地奈德进行干预后b-FGF和NF-κB的表达明显降低（111.61±5.52 vs 126.21±6.46; 110.65±8.71 vs 134.15±9.42; P<0.05），且二者呈正相关性。结论：b-FGF和NF-κB可能与哮喘大鼠气道重塑相关，布地奈德改善哮喘大鼠的气道重塑可能与降低b-FGF和NF-κB的表达有关。［中国当代儿科杂志，2009，11（5）：393-396］

Expression of basic fibroblast growth factor and nuclear factor-κB and the effect of budesonide on their expression in rats with asthma

Objective To study the expression of basic fibroblast growth factor (b-FGF) and nuclear factor-κB (NF-κB) in the airway and the effect of budesonide on their expression in rats with asthma.Methods Forty-five Sprague-Dawley male rats were randomly divided into three group:placebo control,untreated asthma,and budesonide-treated asthma. Asthma was induced by intraperitoneal injection of 10% ovalbumin (OVA) on days 1 and 8 and then challenged by inhalation of 1% OVA aerosol. The budesonide-treated asthma group received an inhalation of budesonide (1 mg) 30 minutes after OVA challenge. The pathological changes of the airway were assessed,and the expression of b-FGF and NF-κB in the airway was assayed by hematoxylin and eosin staining and immunohistochemistry.Results Budesonide treatment alleviated airway injuries. Compared with the control group,b-FGF and NF-κB expression in the airway in the untreated asthma group increased significantly (P<0.05). The budesonide-treated asthma group demonstrated significantly decreased b-FGF (111.61±5.52 vs 126.21±6.46; P<0.05) and NF-κB expression (110.65±8.71 vs 134.15±9.42; P<0.05) in the airway as compared with the untreated asthma group. b-FGF expression was positively correlated to NF-κB expression in the budesonide-treated group.Conclusions b-FGF and NF-κB may be associated with airway remodeling in rats with asthma. Budesonide can improve airway remodeling,possibly by decreasing the expression of b-FGF and NF-κB.