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黃芪甲苷干預(yù)對(duì)哮喘小鼠氣道黏液高分泌的影響

發(fā)布時(shí)間:2018-08-30 16:37
【摘要】:目的:觀察卵蛋白(OVA)誘導(dǎo)哮喘小鼠氣道炎癥及氣道黏液高分泌表現(xiàn)。 方法:清潔級(jí)BALB/c小鼠20只隨機(jī)分為哮喘組(AS組)和生理鹽水對(duì)照組(NS組),每組10只。AS組于第1天、第13天以20μgOVA腹腔注射致敏,第19天始霧化吸入10%OVA激發(fā)連續(xù)5天,末次激發(fā)24小時(shí)后處死小鼠。BALF細(xì)胞總數(shù)、嗜酸性粒細(xì)胞計(jì)數(shù),HE染色觀察肺組織病理學(xué)改變,ELISA檢測(cè)BALF中IL-5水平的變化,阿辛藍(lán)-過(guò)碘酸雪夫(AB-PAS)染色觀察氣道上皮杯狀細(xì)胞及黏液物質(zhì)改變,免疫組織化學(xué)(IHC)檢測(cè)肺組織中黏蛋白5ac (Muc5ac)的表達(dá)水平,Real-time PCR檢測(cè)肺組織中Muc5ac mRNA的表達(dá)水平。 結(jié)果:AS組小鼠氣道炎癥病理評(píng)分、BALF細(xì)胞總數(shù)、嗜酸性粒細(xì)胞計(jì)數(shù)、IL-5水平、氣道上皮杯狀細(xì)胞及黏液物質(zhì)陽(yáng)性相對(duì)著色面積、肺組織Muc5ac蛋白及其mRNA表達(dá)均高于NS組,各組間差異有統(tǒng)計(jì)學(xué)意義(P0.05)。 結(jié)論:哮喘小鼠出現(xiàn)以嗜酸性粒細(xì)胞浸潤(rùn)為主的氣道慢性炎癥和氣道黏液高分泌。 目的:觀察黃芪甲苷干預(yù)對(duì)哮喘小鼠氣道黏液高分泌及IL33表達(dá)的影響,探討其作用機(jī)制。 方法:清潔級(jí)BALB/c小鼠40只隨機(jī)分成4組:生理鹽水對(duì)照組(NS組)、哮喘組(AS組)、黃芪甲苷干預(yù)組(AS+AST-Ⅳ組,50mg·kg-1·d-1體質(zhì)量)、地塞米松組(AS+DEX組,2mg·kg-1·d-1體質(zhì)量),每組10只。哮喘模型制備同第一部分。行BALF細(xì)胞總數(shù)、嗜酸性粒細(xì)胞計(jì)數(shù)、ELISA檢測(cè)BALF中IL-5水平,HE染色觀察小鼠肺組織病理學(xué)變化,AB-PAS染色觀察氣道組織杯狀細(xì)胞、黏液分泌情況,IHC/Real-time PCR檢測(cè)Muc5ac、IL33蛋白及mRNA在氣道和肺組織內(nèi)的表達(dá)。 結(jié)果:AS+AST-Ⅳ組肺組織病理評(píng)分、BALF細(xì)胞總數(shù)、嗜酸性粒細(xì)胞數(shù)、IL-5水平、AB-PAS陽(yáng)性染色面積、Muc5ac及IL33蛋白積分光密度值、Muc5ac及IL33mRNA均較AS減低,差異有統(tǒng)計(jì)學(xué)意義(P0.05); 結(jié)論:黃芪甲苷可抑制哮喘小鼠氣道炎癥,并且降低氣道Muc5ac和IL33的表達(dá)。
[Abstract]:Objective: to observe the airway inflammation and airway mucus hypersecretion in asthmatic mice induced by ovalbumin (OVA). Methods: twenty clean grade BALB/c mice were randomly divided into asthmatic group (AS group) and normal saline control group (NS group). 10 rats in each group were sensitized with 20 渭 gOVA intraperitoneal injection on the 1st day, the 13th day after the injection of 20 渭 gOVA. The total number of BALF cells was killed 24 hours after the last stimulation. Eosinophilic granulocyte count and HE staining were used to observe the changes of lung histopathology. Elisa was used to detect the level of IL-5 in BALF. The changes of goblet cells and mucus in airway epithelium were observed by AB-PAS staining. The expression level of mucin 5ac (Muc5ac) in lung tissue was detected by immunohistochemical (IHC) and Muc5ac mRNA expression in lung tissue was detected by Real-time PCR. Results the total number of BALF cells, the count of eosinophils and IL-5, the positive relative staining area of goblet cells and mucus in the airway epithelium, the expression of Muc5ac protein and mRNA in lung tissue were higher in as group than those in NS group. The differences among groups were statistically significant (P0.05). Conclusion: chronic airway inflammation with eosinophil infiltration and airway mucus hypersecretion were found in asthmatic mice. Aim: to investigate the effect of astragaloside A on airway mucus hypersecretion and IL33 expression in asthmatic mice. Methods: forty clean grade BALB/c mice were randomly divided into 4 groups: normal saline control group (NS group), asthma group (AS group), Astragaloside A intervention group (AS AST- 鈪,

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