IL-33在PM2.5暴露加重變應(yīng)性鼻炎黏膜炎癥反應(yīng)中的作用
發(fā)布時(shí)間:2019-05-18 20:58
【摘要】:目的:本文主要探討1.PM2.5暴露下是否加重變應(yīng)性鼻炎(Allergic Rhinitis,AR)小鼠粘膜炎癥反應(yīng);2.白細(xì)胞介素-33(interleukin-33 IL-33)在其中所起的作用,及可能的途徑。方法:1.采集PM2.5,行理化分析及制備染毒樣品;2.建立變應(yīng)性鼻炎小鼠模型,行行為學(xué)計(jì)分;3.造模成功后,PM2.5干預(yù),建立PM2.5暴露后小鼠模型;4.抗IL-33抗體處理PM2.5暴露下變應(yīng)性鼻炎小鼠模型;取三組小鼠外周血行血涂片計(jì)數(shù)嗜酸性粒細(xì)胞,ELISA檢測(cè)IgE及IL-33水平;取鼻粘膜觀察其形態(tài)學(xué)的改變;鼻粘膜另行western blot檢測(cè)NF-κB表達(dá)水平。結(jié)果:1.PM2.5顆粒染毒樣品制備成功;2.AR小鼠模型建模成功,典型癥狀明顯;3.外周血涂片結(jié)果:AR模型組嗜酸性粒細(xì)胞計(jì)數(shù)低于PM2.5干預(yù)組,P0.05;抗IL-33治療組嗜酸性粒細(xì)胞計(jì)數(shù)低于PM2.5干預(yù)組,P0.05;4.ELISA結(jié)果:AR模型組血清IgE、IL-33水平明顯低于PM2.5干預(yù)組,P0.05;抗IL-33治療組血清IgE、IL-33水平低于PM2.5干預(yù)組,P0.05;5.鼻粘膜HE染色結(jié)果:AR模型組:鼻粘膜上皮結(jié)構(gòu)紊亂,纖毛脫落,粘膜下層可見EOS、中性粒細(xì)胞等炎細(xì)胞浸潤(rùn)。PM2.5干預(yù)組:鼻粘膜上皮細(xì)胞結(jié)構(gòu)不完整,纖毛大量脫落,粘膜下層EOS、中性粒細(xì)胞等炎細(xì)胞浸潤(rùn)明顯,可見組織水腫,腺體增生?笽L-33治療組:鼻粘膜可見基本完整的纖毛結(jié)構(gòu),且上皮細(xì)胞排列較為整齊,輕度炎細(xì)胞浸潤(rùn)。6.Western blot結(jié)果:AR模型組鼻粘膜NF-κB水平低于PM2.5干預(yù)組,P0.05;抗IL-33治療組鼻粘膜NF-κB水平低于PM2.5干預(yù)組,P0.05。結(jié)論:1.PM2.5粒徑小,面積大,活性強(qiáng),成分復(fù)雜,易附帶重金屬、病原微生物、多環(huán)芳烴及其衍生物等有毒、有害物質(zhì)。2.PM2.5可加重變應(yīng)性鼻炎黏膜炎癥反應(yīng)。3.PM2.5暴露下的AR小鼠外周血IL-33水平增高。4.抗IL-33抗體可減輕PM2.5暴露下變應(yīng)性鼻炎黏膜炎癥反應(yīng)。5.IL-33可能通過NF-κB途徑發(fā)揮其作用。
[Abstract]:Objective: to investigate whether the inflammatory reaction of allergic rhinitis (Allergic Rhinitis,AR) mice is aggravated by 1.PM2.5 exposure. The role and possible pathways of IL-33 (interleukin-33 IL-33) in it. Method: 1. PM2.5, was collected for physical and chemical analysis and the samples were prepared. 2. The mouse model of allergic rhinitis was established, and the action score was 3. After successful modeling, PM2.5 intervened to establish the mouse model after PM2.5 exposure. 4. The mice model of allergic rhinitis exposed to PM2.5 was treated with anti-IL-33 antibody, the peripheral blood smears of the three groups were taken to count eosinophils, the levels of IgE and IL-33 were detected by ELISA, and the morphological changes of nasal mucosa were observed. The expression of NF- kappa B was detected by western blot in nasal mucosa. Results: the sample of 1.PM2.5 particles was successfully prepared, the model of 2.AR mice was established successfully, and the typical symptoms were obvious. The results of peripheral blood smear showed that the count of eosinophils in AR model group was lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05). 4.ELISA results: the level of serum IgE,IL-33 in AR model group was significantly lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05 鈮,
本文編號(hào):2480331
[Abstract]:Objective: to investigate whether the inflammatory reaction of allergic rhinitis (Allergic Rhinitis,AR) mice is aggravated by 1.PM2.5 exposure. The role and possible pathways of IL-33 (interleukin-33 IL-33) in it. Method: 1. PM2.5, was collected for physical and chemical analysis and the samples were prepared. 2. The mouse model of allergic rhinitis was established, and the action score was 3. After successful modeling, PM2.5 intervened to establish the mouse model after PM2.5 exposure. 4. The mice model of allergic rhinitis exposed to PM2.5 was treated with anti-IL-33 antibody, the peripheral blood smears of the three groups were taken to count eosinophils, the levels of IgE and IL-33 were detected by ELISA, and the morphological changes of nasal mucosa were observed. The expression of NF- kappa B was detected by western blot in nasal mucosa. Results: the sample of 1.PM2.5 particles was successfully prepared, the model of 2.AR mice was established successfully, and the typical symptoms were obvious. The results of peripheral blood smear showed that the count of eosinophils in AR model group was lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05). 4.ELISA results: the level of serum IgE,IL-33 in AR model group was significantly lower than that in PM2.5 intervention group (P0.05), and that in anti-IL-33 treatment group was lower than that in PM2.5 intervention group (P0.05 鈮,
本文編號(hào):2480331
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