临床耳鼻咽喉头颈外科杂志
臨床耳鼻嚥喉頭頸外科雜誌
림상이비인후두경외과잡지
JOURNAL OF CLINICAL OTORHINOLARYNGOLOGY HEAD AND NECK SURGERY
2009年
14期
649-651,655
,共4页
鼻炎,变应性%碱性成纤维细胞生长因子%丙酸氟替卡松
鼻炎,變應性%堿性成纖維細胞生長因子%丙痠氟替卡鬆
비염,변응성%감성성섬유세포생장인자%병산불체잡송
allergic rhinitis%basic fibroblast growth factor%fluticasone
目的:观察碱性成纤维细胞生长因子(bFGF)在变应性鼻炎(AR)大鼠鼻黏膜组织中的表达情况及丙酸氟替卡松(FP)干预的影响.方法:90只SD大鼠随机分为正常对照组、AR组和FP治疗组,以卵清白蛋白激发法制备AR模型,采用免疫组织化学和RT-PCR法测定鼻黏膜组织中bFGF蛋白和mRNA 的表达情况.结果:AR组bFGF蛋白和mRNA的表达水平显著高于正常对照组(P<0.01),FP治疗组显著低于AR组(P<0.01),但与正常对照组相比仍较高(P<0.01) ,上皮细胞为主要表达细胞.结论:bFGF参与了AR的发病机制, FP可抑制bFGF蛋白和mRNA的表达增加效应,这可能是FP抑制AR鼻黏膜重塑的重要机制之一.
目的:觀察堿性成纖維細胞生長因子(bFGF)在變應性鼻炎(AR)大鼠鼻黏膜組織中的錶達情況及丙痠氟替卡鬆(FP)榦預的影響.方法:90隻SD大鼠隨機分為正常對照組、AR組和FP治療組,以卵清白蛋白激髮法製備AR模型,採用免疫組織化學和RT-PCR法測定鼻黏膜組織中bFGF蛋白和mRNA 的錶達情況.結果:AR組bFGF蛋白和mRNA的錶達水平顯著高于正常對照組(P<0.01),FP治療組顯著低于AR組(P<0.01),但與正常對照組相比仍較高(P<0.01) ,上皮細胞為主要錶達細胞.結論:bFGF參與瞭AR的髮病機製, FP可抑製bFGF蛋白和mRNA的錶達增加效應,這可能是FP抑製AR鼻黏膜重塑的重要機製之一.
목적:관찰감성성섬유세포생장인자(bFGF)재변응성비염(AR)대서비점막조직중적표체정황급병산불체잡송(FP)간예적영향.방법:90지SD대서수궤분위정상대조조、AR조화FP치료조,이란청백단백격발법제비AR모형,채용면역조직화학화RT-PCR법측정비점막조직중bFGF단백화mRNA 적표체정황.결과:AR조bFGF단백화mRNA적표체수평현저고우정상대조조(P<0.01),FP치료조현저저우AR조(P<0.01),단여정상대조조상비잉교고(P<0.01) ,상피세포위주요표체세포.결론:bFGF삼여료AR적발병궤제, FP가억제bFGF단백화mRNA적표체증가효응,저가능시FP억제AR비점막중소적중요궤제지일.
Objective:To investigate the effects of fluticasone on expression of basic fibroblast growth factor and mRNA in allergic rhinitis rats. Method:Ninety Sprague-Dawley rats were randomly divided into three groups(n = 30 for each) , including AR group, control group and fluticasone treatment group. In this experiment , the rat model of AR was established by the ovalbumin challenge methods. The expression of the protein of basic fibroblast growth factor and mRNA were detected with immunohistochemistry methods and in RT-PCR methods. Result:The protein and mRNA expression of basic fibroblast growth factor in nasal tissue was significantly higher in the AR group than that in control group(P<0.01),and it was much lower in the treatment group than that in the AR group(P<0.01) ibut still higher than that in the control group(P<0.01). The epithelial cell was the chief expression cell. Conclusion:The basic fibroblast growth factor participates in the pathogenesis of AR ,and inhaled fluticasone can significantly inhabit the expression of the protein and mRNA of basic fibroblast growth factor in the chronic stage of AR,thus preventing the airway remodeling.