MKK34多肽对HDM哮喘小鼠气道β-catenin表达及分布的影响
发布时间：2018-07-29 15:23
【摘要】：目的:观察MKK34多肽(TSLP碳端α螺旋区域)对屋尘螨(HDM)哮喘小鼠气道炎症及气道上皮细胞连接蛋白β-catenin的影响。方法:将32只BALB/c小鼠随机分为4组。哮喘组每周连续5 d滴鼻给予HDM,预处理组在给予HDM前1 h滴鼻给予MKK34多肽,8周后,动物肺功能测定和病理染色来评估哮喘的情况,检测各组小鼠的肺泡灌洗液IL-4、IFN-γ及血清Ig E,用免疫组化及Western blot测定肺组织β-catenin的分布和表达及p-ERK1/2、t-ERK1/2的表达。结果:HDM哮喘组气道反应性、肺泡灌洗液IL-4和血清Ig E均较对照组增高,MKK34预处理组较哮喘组上述指标都有所改善。肺组织HE染色示哮喘组具有气道炎症的典型病变,而MKK34预处理组炎症明显轻于哮喘组,免疫组化及Western blot结果示,对照组在气道上皮细胞的细胞膜连接处紧密的分布着β-catenin蛋白,而哮喘组β-catenin分布混乱、减少,MKK34预处理组能减少β-catenin的破坏,在哮喘组p-ERK1/2表达明显增加,MKK34多肽预处理组较哮喘组减少。结论:MKK34多肽可能通过抑制ERK的磷酸化来改善HDM哮喘小鼠的气道炎症及气道上皮细胞连接蛋白β-catenin的破坏。
[Abstract]:Aim: to observe the effect of MKK34 polypeptide (TSLP carbon terminal 伪 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- 纬 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.
【作者单位】： 南方医科大学南方医院呼吸与危重症医学科慢性气道疾病实验室;
【基金】：国家自然科学基金(编号:81270087,81470228,81670026) 国家重点研发计划(编号:2016YFC0905803)
【分类号】：R562.25
本文编号：2153109
[Abstract]:Aim: to observe the effect of MKK34 polypeptide (TSLP carbon terminal 伪 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- 纬 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.
【作者单位】： 南方医科大学南方医院呼吸与危重症医学科慢性气道疾病实验室;
【基金】：国家自然科学基金(编号:81270087,81470228,81670026) 国家重点研发计划(编号:2016YFC0905803)
【分类号】：R562.25
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