雾化吸入灭活草分枝杆菌降低哮喘小鼠核因子κB及细胞间黏附分子1的表达

发布时间：2018-03-22 22:06

本文选题：哮喘　切入点：灭活草分枝杆菌　出处：《中国病理生理杂志》2014年02期 　论文类型：期刊论文

【摘要】：目的:研究雾化吸入灭活草分枝杆菌对支气管哮喘小鼠气道炎症,以及哮喘肺组织中核因子κB(NF-κB)、细胞间黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)的影响,探讨雾化吸入灭活草分枝杆菌防治哮喘的机制。方法:将24只雄性BALB/c小鼠按随机数字表法分为3组,每组8只:正常对照组(A)、哮喘模型组(B)和治疗组(C)。以鸡卵清蛋白致敏制造小鼠支气管哮喘模型。C组在激发后给予雾化吸入灭活草分枝杆菌治疗5 d,每天1次。各组动物处死后提取肺组织和支气管肺泡灌洗液(BALF)。进行病理HE染色及AB-PAS染色观察气道炎症浸润及黏液分泌情况,并行病理半定量分析。对BALF中炎症细胞进行分类计数。实时荧光定量PCR检测肺组织NF-κB、ICAM-1和VCAM-1的mRNA表达水平。结果:治疗组嗜酸性粒细胞比例低于模型组(P0.05),气道炎症病变及黏液分泌情况较模型组减轻(P0.05,P0.01)。哮喘模型组的肺组织中NF-κB mRNA含量与正常组相比显著升高(P0.01),而治疗组肺组织中的NF-κB mRNA含量明显低于模型组(P0.05);模型组的ICAM-1 mRNA水平比正常组高(P0.05),但治疗后明显降低(P0.01);VCAM-1的mRNA水平在各组间无显著差异。相关性检验发现小鼠肺组织中VCAM-1的mRNA与ICAM-1的mRNA呈明显正相关(r=0.84,P0.01),但NF-κB的mRNA与ICAM-1的mRNA、VCAM-1的mRNA无明显相关性(均P0.05)。结论:雾化吸入草分枝杆菌对支气管哮喘小鼠气道炎症及黏液分泌有抑制作用;NF-κB参与哮喘发病过程,雾化吸入灭活草分枝杆菌降低哮喘小鼠的NF-κB水平。同时雾化吸入灭活草分枝杆菌可降低黏附分子尤其是ICAM-1的表达,是其控制炎症的另一个重要机制。
[Abstract]:Objective: to study the effects of aerosol inhalation of inactivated mycobacterium on airway inflammation in asthmatic mice and the effects of nuclear factor 魏 B (NF- B) NF- 魏 B, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in lung tissues of asthmatic mice. Methods: 24 male BALB/c mice were divided into 3 groups according to random digital table method. Eight rats in each group: normal control group, asthma model group (B) and treatment group. The mice bronchial asthma model was sensitized with chicken ovalbumin. Group C was treated with aerosol inhalation inactivated mycobacterium once a day for 5 days after stimulation. The lung tissue and bronchoalveolar lavage fluid (BALF) were extracted from the animals of the group A, and the inflammatory infiltration and mucus secretion in the airway were observed by HE staining and AB-PAS staining. Pathological semi-quantitative analysis was performed. The inflammatory cells in BALF were classified and counted. Real-time quantitative PCR was used to detect the mRNA expression of NF- 魏 BnICAM-1 and VCAM-1 in lung tissue. Results: the percentage of eosinophils in the treatment group was lower than that in the model group (P 0.05), and airway inflammation in the treatment group was lower than that in the model group (P 0.05). The level of NF- 魏 B mRNA in lung tissue of asthmatic model group was significantly higher than that of normal group, while the content of NF- 魏 B mRNA in lung tissue of treatment group was significantly lower than that of model group, and the level of ICAM-1 mRNA in model group was significantly lower than that in model group. The level of VCAM-1 mRNA was significantly decreased after treatment. The correlation test showed that there was a positive correlation between mRNA of VCAM-1 and mRNA of ICAM-1 in lung tissue of mice, but there was no significant correlation between mRNA of NF- 魏 B and mRNA of mRNAVCAM-1 of ICAM-1. Conclusion: aerosol inhalation of Mycobacterium vulgaris can inhibit airway inflammation and mucus secretion in asthmatic mice. NF- 魏 B is involved in the pathogenesis of asthma. Aerosol inhalation of inactivated mycobacterium can reduce the level of NF- 魏 B in asthmatic mice, and aerosolized inhalation of Mycobacterium inactivated can reduce the expression of adhesion molecules, especially ICAM-1, which is another important mechanism for the control of inflammation.
【作者单位】：广西医科大学第一附属医院呼吸内科;
【基金】：国家自然科学基金资助项目(No.81360007)
【分类号】：R562.25

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