【摘要】：目的:觀察MKK34多肽(TSLP碳端α螺旋區(qū)域)對(duì)屋塵螨(HDM)哮喘小鼠氣道炎癥及氣道上皮細(xì)胞連接蛋白β-catenin的影響。方法:將32只BALB/c小鼠隨機(jī)分為4組。哮喘組每周連續(xù)5 d滴鼻給予HDM,預(yù)處理組在給予HDM前1 h滴鼻給予MKK34多肽,8周后,動(dòng)物肺功能測(cè)定和病理染色來(lái)評(píng)估哮喘的情況,檢測(cè)各組小鼠的肺泡灌洗液IL-4、IFN-γ及血清Ig E,用免疫組化及Western blot測(cè)定肺組織β-catenin的分布和表達(dá)及p-ERK1/2、t-ERK1/2的表達(dá)。結(jié)果:HDM哮喘組氣道反應(yīng)性、肺泡灌洗液IL-4和血清Ig E均較對(duì)照組增高,MKK34預(yù)處理組較哮喘組上述指標(biāo)都有所改善。肺組織HE染色示哮喘組具有氣道炎癥的典型病變,而MKK34預(yù)處理組炎癥明顯輕于哮喘組,免疫組化及Western blot結(jié)果示,對(duì)照組在氣道上皮細(xì)胞的細(xì)胞膜連接處緊密的分布著β-catenin蛋白,而哮喘組β-catenin分布混亂、減少,MKK34預(yù)處理組能減少β-catenin的破壞,在哮喘組p-ERK1/2表達(dá)明顯增加,MKK34多肽預(yù)處理組較哮喘組減少。結(jié)論:MKK34多肽可能通過(guò)抑制ERK的磷酸化來(lái)改善HDM哮喘小鼠的氣道炎癥及氣道上皮細(xì)胞連接蛋白β-catenin的破壞。
[Abstract]:Aim: to observe the effect of MKK34 polypeptide (TSLP carbon terminal 偽 helical region) on airway inflammation and airway epithelial cell junction protein 尾 -catenin in (HDM) asthmatic mice. Methods: 32 BALB/c mice were randomly divided into 4 groups. The asthmatic group was given intranasal administration of MKK34 for 5 days a week, and the preconditioning group was given MKK34 polypeptide 8 weeks before HDM was given. The lung function and pathological staining were used to evaluate the asthma status in the preconditioning group. The IL-4 IFN- 緯 and serum IgE in alveolar lavage fluid of each group were detected. The distribution and expression of 尾 -catenin and the expression of p-ERK1 / 2 -ERK1 / 2 in lung tissue were determined by immunohistochemistry and Western blot. Results compared with the control group, the airway reactivity, alveolar lavage fluid (IL-4) and serum IgE in the control group were higher than those in the control group. Lung tissue HE staining showed that asthma group had typical pathological changes of airway inflammation, while the inflammation of MKK34 pretreatment group was significantly less than that of asthma group. Immunohistochemical and Western blot results showed that 尾 -catenin protein was closely distributed in the membrane junction of airway epithelial cells in the control group. However, the distribution of 尾 -catenin in asthma group was confused, and the damage of 尾 -catenin was reduced in MKK34 preconditioning group. The expression of p-ERK1/2 in asthma group was significantly increased compared with that in asthma group. Conclusion the molecular weight MKK34 peptide may inhibit the phosphorylation of ERK to ameliorate the airway inflammation and the destruction of 尾 -catenin in the airway epithelial cells of HDM asthmatic mice.
【作者單位】： 南方醫(yī)科大學(xué)南方醫(yī)院呼吸與危重癥醫(yī)學(xué)科慢性氣道疾病實(shí)驗(yàn)室;
【基金】：國(guó)家自然科學(xué)基金(編號(hào):81270087,81470228,81670026) 國(guó)家重點(diǎn)研發(fā)計(jì)劃(編號(hào):2016YFC0905803)
【分類號(hào)】：R562.25

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