过敏原对哮喘患儿肺功能影响的动态观察分析.DOCVIP

遗传性肥胖对气道炎症和纤维化的影 王冬娟 黄英 柴水 宋晔 崔欢欢 肖晓秋 （重庆医科大学附属儿童医院呼吸中心，重庆400014） 中国图书分类号 作者简介：王冬娟（1985年-），女，在读硕士，主要从事儿童肥胖与哮喘相关机制的研究，E-mail：wangdongjuan0816@163.com；通讯作者及指导教师：黄英（1957年-），女，教授，硕士生导师，主要从事儿童肥胖与哮喘相关机制的研究，E-mail：huangying62@163.com【摘要】目的 通过肥胖小鼠模型，探讨肥胖对气道炎症和纤维化的影。方法：应用ob/ob基因敲除C57肥胖小鼠模型，喂养至5个月。进行肺组织HE染色、α-SMA免疫组化。结果：在小鼠达到肥胖标准的前提下：（1）肥胖小鼠肺组织中炎症细胞浸润明显增加：主要集中在支气管周围，比正常组明显增加（P＜0.05），而肺泡周围增加并不明显（P＞0.05）。（2）肥胖小鼠肺组织出现不同程度的纤维化：支气管周围纤维化程度较正常组明显高。（3）肥胖小鼠肺组织中MMP-9 蛋白表达明显升高。结论：肥胖小鼠模型显示，肥胖可以增加肺组织炎症和纤维化。 关键词：肥胖 气道炎症 纤维化 哮喘To observe the influence of genetically obese on airway inflammation and fibrosis 【 Abstact】Objective : To explore the effect of obesity on airway inflammation and fibrosis observe the obese mouse model. Methods: The model is ob/ob gene knockout induced obesity, feeding to 5 months. HE staining, immunohistochemical of alpha SMA, and the protein detection of MMP - 9 are used. Results: Under the premise of meet the standard of obesity: (1) the infiltration of inflammatory cells in the lung tissue are obviously increased obesity mouse model: mainly concentrated around the bronchi in the ob/ob obesity mice, and is increased compared to the normal group (P 0.05), but the inflammatory cells around the alveoli is not obvious (P 0.05). (2) There is different degree of lung fibrosis on the obesity mouse model: significantly higher than normal group around the bronchial in the ob/ob gene knockout induced obesity mice. (3) The expression of MMP - 9 in lung tissue is significantly increased in the obesity mouse model. Conclusion: The ob/ob gene knockout induced obesity mice showed that obesity can increase the inflammation and fibrosis of the lung tissue. [Key words] obesity airway inflammation fibrosis asthma 肥胖已经成为一种重要的代谢性疾病，其发病率逐年上升，严重威胁着人类的健康。 而且肥胖已经成为全球疾病负担的第六大危险因素【1】，与多种疾病的发生发展密切相关，如心血管疾病中动脉粥样硬化、高血压等，呼吸系统中COPD以及哮喘等。06年GINA已经将肥胖列为哮喘的独立危险因素之一。 肥胖对呼吸系统