中华耳鼻咽喉头颈外科杂志
中華耳鼻嚥喉頭頸外科雜誌
중화이비인후두경외과잡지
CHINESE JOURNAL OF OTORHINOLARYNGOLOGY HEAD AND NECK SURGERY
2011年
1期
59-62
,共4页
李钦%孔平%武彩霞%孙崇伟%陈彦林%许晓群%张大良
李欽%孔平%武綵霞%孫崇偉%陳彥林%許曉群%張大良
리흠%공평%무채하%손숭위%진언림%허효군%장대량
疾病模型,动物%鼻炎,变应性,常年性%干扰素Ⅱ型%大鼠%转化生长因子β%Smad蛋白质类
疾病模型,動物%鼻炎,變應性,常年性%榦擾素Ⅱ型%大鼠%轉化生長因子β%Smad蛋白質類
질병모형,동물%비염,변응성,상년성%간우소Ⅱ형%대서%전화생장인자β%Smad단백질류
Disease models,animal%Rhinitis,allergic,perennial%Interferon type Ⅱ%Rats%Transforming growth factor beta 1%Smad proteins
目的 探讨鼻腔吸入γ干扰素(interferon gamma,IFN-y)对大鼠变应性鼻炎(allergicrhinitis,AR)转化生长因子β1(transforming growth factor-β1,TGF-β1)/Smad信号通路的影响.方法 采用卵白蛋白、氢氧化铝建立大鼠AR鼻黏膜重塑模型.分为AR模型组(B组)、IFN-γ组(C组),每组10只大鼠,分别于第4～10周,每周2次每只每侧鼻腔滴入磷酸盐缓冲液50μl、IFN-γ 1μg,另设阴性对照组(A组)大鼠10只,于最后一次吸入结束后24 h取鼻黏膜组织检测TGF-β1蛋白及TGF-β1、Smad2、Smad3、Smad7 mRNA的表达.结果 C组鼻腔黏膜组织中TGF-β1、Smad2、Smad3mRNA相对表达强度分别为0.59±0.04、0.39±0.08、0.46±0.15,明显低于B组的0.82±0.12、0.70±0.18、0.95±0.26,差异有统计学意义(q值分别为3.15、4.47、3.03,P值均<0.05);C组鼻腔黏膜组织中Smad7 mRNA相对表达强度为0.31±0.05,明显高于B组的0.25±0.06,差异有统计学意义(q=2.98,P<0.05).免疫组化显示B组鼻腔黏膜组织中TGF-β1蛋白表达增加,而C组的表达减少.结论 鼻腔吸入IFN-γ通过抑制AR大鼠鼻黏膜组织TGF-β1、Smad2、Smad3的过度表达,上调Smad7的表达,从而阻断TGF-β1/Smad信号通路,明显减轻了大鼠AR鼻黏膜的重塑.
目的 探討鼻腔吸入γ榦擾素(interferon gamma,IFN-y)對大鼠變應性鼻炎(allergicrhinitis,AR)轉化生長因子β1(transforming growth factor-β1,TGF-β1)/Smad信號通路的影響.方法 採用卵白蛋白、氫氧化鋁建立大鼠AR鼻黏膜重塑模型.分為AR模型組(B組)、IFN-γ組(C組),每組10隻大鼠,分彆于第4～10週,每週2次每隻每側鼻腔滴入燐痠鹽緩遲液50μl、IFN-γ 1μg,另設陰性對照組(A組)大鼠10隻,于最後一次吸入結束後24 h取鼻黏膜組織檢測TGF-β1蛋白及TGF-β1、Smad2、Smad3、Smad7 mRNA的錶達.結果 C組鼻腔黏膜組織中TGF-β1、Smad2、Smad3mRNA相對錶達彊度分彆為0.59±0.04、0.39±0.08、0.46±0.15,明顯低于B組的0.82±0.12、0.70±0.18、0.95±0.26,差異有統計學意義(q值分彆為3.15、4.47、3.03,P值均<0.05);C組鼻腔黏膜組織中Smad7 mRNA相對錶達彊度為0.31±0.05,明顯高于B組的0.25±0.06,差異有統計學意義(q=2.98,P<0.05).免疫組化顯示B組鼻腔黏膜組織中TGF-β1蛋白錶達增加,而C組的錶達減少.結論 鼻腔吸入IFN-γ通過抑製AR大鼠鼻黏膜組織TGF-β1、Smad2、Smad3的過度錶達,上調Smad7的錶達,從而阻斷TGF-β1/Smad信號通路,明顯減輕瞭大鼠AR鼻黏膜的重塑.
목적 탐토비강흡입γ간우소(interferon gamma,IFN-y)대대서변응성비염(allergicrhinitis,AR)전화생장인자β1(transforming growth factor-β1,TGF-β1)/Smad신호통로적영향.방법 채용란백단백、경양화려건립대서AR비점막중소모형.분위AR모형조(B조)、IFN-γ조(C조),매조10지대서,분별우제4～10주,매주2차매지매측비강적입린산염완충액50μl、IFN-γ 1μg,령설음성대조조(A조)대서10지,우최후일차흡입결속후24 h취비점막조직검측TGF-β1단백급TGF-β1、Smad2、Smad3、Smad7 mRNA적표체.결과 C조비강점막조직중TGF-β1、Smad2、Smad3mRNA상대표체강도분별위0.59±0.04、0.39±0.08、0.46±0.15,명현저우B조적0.82±0.12、0.70±0.18、0.95±0.26,차이유통계학의의(q치분별위3.15、4.47、3.03,P치균<0.05);C조비강점막조직중Smad7 mRNA상대표체강도위0.31±0.05,명현고우B조적0.25±0.06,차이유통계학의의(q=2.98,P<0.05).면역조화현시B조비강점막조직중TGF-β1단백표체증가,이C조적표체감소.결론 비강흡입IFN-γ통과억제AR대서비점막조직TGF-β1、Smad2、Smad3적과도표체,상조Smad7적표체,종이조단TGF-β1/Smad신호통로,명현감경료대서AR비점막적중소.
Objective To investigate the effects of intranasal interferon gamma (IFN-γ) on nasal mucosa remodeling and expression of transforming growth factor-β1 ( TGF-β1 ), Smad2, Smad3, Smad7 in allergic rhinitis (AR) rat model. Methods Ovalbumin (OVA) and aluminum hydroxide were used to construct the AR model. Thirty AR rats were randomly divided into positive control group (group B, n =10), IFN-γ treatment group( group C, n = 10) and negative control group( normal rats, n = 10). After the AR models were built, 50μl PBS, 1 μg IFN-γ was dropped into the nasal cavity of each rat in group B and group C, from the fouth week to tenth week, twice a week. The nasal mucosa was collected on day 71 in order to observe the pathologic changes, and the expression of TGF-β1, TGF-β1 mRNA, Smad2 mRNA,Smad3 mRNA and Smad7 mRNA by immunohistochemistry and reverse transcriptase-polymerase chain reaction. Results Decreases of TGF-β1, Smad2 and Smad3 mRNA were seen in nasal tissue of group C (0. 59 ±0. 04, 0. 39 ±0. 08, 0. 46 ±0. 15) as compared with group B (0. 82 ±0. 12, 0. 70 ±0. 18, 0. 95 ±0. 26) , the differences were significant ( q value were 3.15, 4. 47, 3.03, all P ＜ 0. 05 ). The levels of Smad7 mRNA expression increased significantly ( q = 2.98, P ＜ 0. 05 ) in group C ( 0. 31 ± 0. 05 ) as compared with group B ( 0.25±0.06). Immunohistochemistry showed significant decrease of TGF-β1expression in the nasal tissue of group C much lesser than that in group B. Conclusions Intranasal IFN-γcould decrease the expression of TGF-β1, TGF-β1 mRNA, Smad2 mRNA, Smad3 mRNA, increase the expression of Smad7 mRNA in AR rats model and inhibit the nasal mucosa remodeling.
