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
2009年
3期
242-245
,共4页
糖皮质激素类%鼻炎,变应性,常年性%氯化物通道%黏蛋白类
糖皮質激素類%鼻炎,變應性,常年性%氯化物通道%黏蛋白類
당피질격소류%비염,변응성,상년성%록화물통도%점단백류
Glucocorticoids%Rhinitis,allergic,perennial%Chloride channels%Mucins
目的 研究变应性鼻炎大鼠模型鼻黏膜钙激活氯通道CLCA3和黏蛋白Muc5ac的表达及糖皮质激素对其的影响.方法 30只SD大鼠随机分成变应性鼻炎组、地塞米松干预组和对照组,用逆转录聚合酶链反应法(reverse transcription-polymerase chain reaction,RT-PCR)和免疫组化法分别检测大鼠鼻黏膜CLCA3 mRNA和Muc5ac蛋白的表达.结果 变应性鼻炎组大鼠鼻黏膜CLCA3mRNA和Muc5ac蛋白表达分别为0.344±0.127、1.401±0.574,均较对照组(分别为0.000±0.000、0.391±0.177)明显增加(t=8.565、5.317,P值均<0.01),且变应性鼻炎组中CLCA3 mRNA表达与Muc5ac蛋白的表达呈直线正相关(r=0.813,P<0.05);地塞米松组中CLCA3 mRNA和MucSac蛋白的表达较变应性鼻炎组均明显减少(t=3.102、2.226,P值均<0.05).结论 变应性鼻炎大鼠鼻黏膜CLCA3基因表达上调与黏液高分泌同时存在,CLCA3可能在变应性鼻炎鼻黏膜黏液高分泌中起重要作用;糖皮质激素可显著抑制CLCA3及黏蛋白的合成.
目的 研究變應性鼻炎大鼠模型鼻黏膜鈣激活氯通道CLCA3和黏蛋白Muc5ac的錶達及糖皮質激素對其的影響.方法 30隻SD大鼠隨機分成變應性鼻炎組、地塞米鬆榦預組和對照組,用逆轉錄聚閤酶鏈反應法(reverse transcription-polymerase chain reaction,RT-PCR)和免疫組化法分彆檢測大鼠鼻黏膜CLCA3 mRNA和Muc5ac蛋白的錶達.結果 變應性鼻炎組大鼠鼻黏膜CLCA3mRNA和Muc5ac蛋白錶達分彆為0.344±0.127、1.401±0.574,均較對照組(分彆為0.000±0.000、0.391±0.177)明顯增加(t=8.565、5.317,P值均<0.01),且變應性鼻炎組中CLCA3 mRNA錶達與Muc5ac蛋白的錶達呈直線正相關(r=0.813,P<0.05);地塞米鬆組中CLCA3 mRNA和MucSac蛋白的錶達較變應性鼻炎組均明顯減少(t=3.102、2.226,P值均<0.05).結論 變應性鼻炎大鼠鼻黏膜CLCA3基因錶達上調與黏液高分泌同時存在,CLCA3可能在變應性鼻炎鼻黏膜黏液高分泌中起重要作用;糖皮質激素可顯著抑製CLCA3及黏蛋白的閤成.
목적 연구변응성비염대서모형비점막개격활록통도CLCA3화점단백Muc5ac적표체급당피질격소대기적영향.방법 30지SD대서수궤분성변응성비염조、지새미송간예조화대조조,용역전록취합매련반응법(reverse transcription-polymerase chain reaction,RT-PCR)화면역조화법분별검측대서비점막CLCA3 mRNA화Muc5ac단백적표체.결과 변응성비염조대서비점막CLCA3mRNA화Muc5ac단백표체분별위0.344±0.127、1.401±0.574,균교대조조(분별위0.000±0.000、0.391±0.177)명현증가(t=8.565、5.317,P치균<0.01),차변응성비염조중CLCA3 mRNA표체여Muc5ac단백적표체정직선정상관(r=0.813,P<0.05);지새미송조중CLCA3 mRNA화MucSac단백적표체교변응성비염조균명현감소(t=3.102、2.226,P치균<0.05).결론 변응성비염대서비점막CLCA3기인표체상조여점액고분비동시존재,CLCA3가능재변응성비염비점막점액고분비중기중요작용;당피질격소가현저억제CLCA3급점단백적합성.
Objective To investigate the expression of CLCA3 and Muc5ac in nasal mucosa in allergic rhinitis rats and the effects of glucocorticoid on its expression. Methods Thirty SD rats were randomly divided into allergic rhinitis group, dexamethasone group and control group. Expression of CLCA3 mRNA and Muc5ac protein in nasal mucosa were detected by RT-PCR and immunohistochemical assay, respectively. Results CLCA3 mRNA and Muc5ac protein in allergic rhinitis group were significantly higher than those in control group (t = 8.565、5.317, P < 0.01, respectively). The increased expression of CLCA3 mRNA in allergic rhinitis group was well correlated with the expression of MucSae protein and the correlation coefficient was 0.813 (P < 0.05). After treatment with dexamethasone, the expression of CLCA3 mRNA and Muc5ae protein was notably lower than that in allergic rhinitis group (t = 3.102,2.226, P < 0.05, respectively). Conclusions The stronger gene expression of CLCA3 exists, complicated with mucus overproduction in the nasal mucosa of allergic rhinitis rats. CLCA3 expression may play a pivotal role in mucus overproduction in allergic rhinitis. Dexamethasone substantially downregulatas the expression of CLCA3 mRNA and Muc5ac protein.
