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
2014年
4期
283-287
,共5页
祁雪萍%索利敏%赵长青%杨平常
祁雪萍%索利敏%趙長青%楊平常
기설평%색리민%조장청%양평상
鼻炎,变应性,常年性%膜蛋白质类%疾病模型,动物%小鼠
鼻炎,變應性,常年性%膜蛋白質類%疾病模型,動物%小鼠
비염,변응성,상년성%막단백질류%질병모형,동물%소서
Rhinitis,allergic,perennial%Membrane proteins%Disease models,animal%Mice
目的 探索T细胞免疫球蛋白黏蛋白分子4 (T cell immunoglobulin and mucin domain molecule4,TIM4)在变应性鼻炎(allergic rhinitis,AR)发病中的作用机制,为AR的治疗提供新思路和新靶点.方法 BALB/C雄性实验小鼠21只完全随机平均分为3组,分别为对照组、AR组及TIM4抗体干预组.AR模型采用卵清蛋白(ovalbumin,OVA)进行基础致敏和鼻腔局部滴鼻激发;采用行为学观察结合免疫学及鼻黏膜HE染色进行AR评估和监测.通过免疫荧光和反转录聚合酶链反应(reverse transcription polymerase chain reaction,RT-PCR)方法,研究TIM4在不同组别小鼠鼻黏膜局部的表达.以SPSS 18.0软件进行统计结果的数据分析.结果 小鼠AR模型制作成功.AR组、对照组、TIM4抗体干预组小鼠鼻黏膜TIM4 mRNA的相对表达量分别为16.29±3.80、0.51 ±0.60、1.64±0.98,3组差异有统计学意义(F=46.56,P＜0.05);AR组显著高于对照组和TIM4抗体干预组,差异有统计学意义(t值分别为8.650、8.027,P值均＜0.05);而对照组与TIM4抗体干预组之间TIM4mRNA表达差异无统计学意义(t=-0.623,P＞0.05).AR小鼠鼻黏膜局部高表达TIM4,其表达部位主要集中在假复层纤毛柱状上皮下层.结论 TIM4在AR发病过程中可能发挥了重要的作用,有效抑制TIM4的表达,可能可以延缓或部分逆转AR的病理过程.
目的 探索T細胞免疫毬蛋白黏蛋白分子4 (T cell immunoglobulin and mucin domain molecule4,TIM4)在變應性鼻炎(allergic rhinitis,AR)髮病中的作用機製,為AR的治療提供新思路和新靶點.方法 BALB/C雄性實驗小鼠21隻完全隨機平均分為3組,分彆為對照組、AR組及TIM4抗體榦預組.AR模型採用卵清蛋白(ovalbumin,OVA)進行基礎緻敏和鼻腔跼部滴鼻激髮;採用行為學觀察結閤免疫學及鼻黏膜HE染色進行AR評估和鑑測.通過免疫熒光和反轉錄聚閤酶鏈反應(reverse transcription polymerase chain reaction,RT-PCR)方法,研究TIM4在不同組彆小鼠鼻黏膜跼部的錶達.以SPSS 18.0軟件進行統計結果的數據分析.結果 小鼠AR模型製作成功.AR組、對照組、TIM4抗體榦預組小鼠鼻黏膜TIM4 mRNA的相對錶達量分彆為16.29±3.80、0.51 ±0.60、1.64±0.98,3組差異有統計學意義(F=46.56,P＜0.05);AR組顯著高于對照組和TIM4抗體榦預組,差異有統計學意義(t值分彆為8.650、8.027,P值均＜0.05);而對照組與TIM4抗體榦預組之間TIM4mRNA錶達差異無統計學意義(t=-0.623,P＞0.05).AR小鼠鼻黏膜跼部高錶達TIM4,其錶達部位主要集中在假複層纖毛柱狀上皮下層.結論 TIM4在AR髮病過程中可能髮揮瞭重要的作用,有效抑製TIM4的錶達,可能可以延緩或部分逆轉AR的病理過程.
목적 탐색T세포면역구단백점단백분자4 (T cell immunoglobulin and mucin domain molecule4,TIM4)재변응성비염(allergic rhinitis,AR)발병중적작용궤제,위AR적치료제공신사로화신파점.방법 BALB/C웅성실험소서21지완전수궤평균분위3조,분별위대조조、AR조급TIM4항체간예조.AR모형채용란청단백(ovalbumin,OVA)진행기출치민화비강국부적비격발;채용행위학관찰결합면역학급비점막HE염색진행AR평고화감측.통과면역형광화반전록취합매련반응(reverse transcription polymerase chain reaction,RT-PCR)방법,연구TIM4재불동조별소서비점막국부적표체.이SPSS 18.0연건진행통계결과적수거분석.결과 소서AR모형제작성공.AR조、대조조、TIM4항체간예조소서비점막TIM4 mRNA적상대표체량분별위16.29±3.80、0.51 ±0.60、1.64±0.98,3조차이유통계학의의(F=46.56,P＜0.05);AR조현저고우대조조화TIM4항체간예조,차이유통계학의의(t치분별위8.650、8.027,P치균＜0.05);이대조조여TIM4항체간예조지간TIM4mRNA표체차이무통계학의의(t=-0.623,P＞0.05).AR소서비점막국부고표체TIM4,기표체부위주요집중재가복층섬모주상상피하층.결론 TIM4재AR발병과정중가능발휘료중요적작용,유효억제TIM4적표체,가능가이연완혹부분역전AR적병리과정.
Objective To investigate the role of TIM4 (T cell immunoglobulin and mucin domainmolecule 4) in the pathogenesis of allergic rhinitis (AR) in mice,and to identify a novel therapeutic target for the treatment of AR.Methods Twenty-one male BALB/C mice of clean grade were divided into three groups randomly (n =7 per group) including control,AR and anti-TIM4 antibody treatment groups.In order to induce upper airway allergic inflammation,the mice from AR and anti-TIM4 antibody treatment groups were sensitized by intraperitoneal injection followed by intranasal challenge with ovalbumin.Before the ovalbumin challenge,a group of mice was treated with anti-TIM4 antibody.To assess the AR model,behavioral observation with immunological assessments and HE staining of nasal tissues were performed.The TIM4 expression in nasal tissues in different groups of mice were assessed by immunofluorescence and RTPCR.SPSS18.0 software was used to analyze the data.Results The AR model in mice was successfully established as shown by behavioral observation and immunological evaluation.RT-PCR assays showed the relative expression of TIM4 mRNA in nasal mucosa of AR,control and anti-TIM4 antibody treatment mice was 16.29 ±3.80,0.51 ±0.60,1.64 ±0.98,respectively.There was statistically significant differencea mong three group (F =46.56,P ＜ 0.05).The expression of TIM4 in AR group was significantly higher than those in control group (t =8.650,P ＜ 0.05) and anti-TIM4 group (t =8.027,P ＜ 0.05).The expression of TIM4 was significantly reduced in the anti-TIM4 antibody group,as well as control group (t =-0.623,P ＞ 0.05).More expression of TIM4 was detected in local nasal tissues of AR mice,mainly located below the pseudostratified ciliated columnar epithelium.Conclusions TIM4 plays a crucial role in the pathogenesis of AR.Effective inhibition of TIM4 expression can partially reverse the pathological changes of AR.
