香烟烟雾对支气管哮喘大鼠气道上皮瘦素表达的影响  

Influence of cigarette smoke on expression of leptin in airway epithelium of asthmatic rats

作　　者：陈碧 韩方方 朱洁晨 张毛为 张晓娇 刘文静 李元芹 赵力 朱述阳 Chen Bi, Han Fangfang, Zhu Jiechen, Zhang Maowei, Zhang Xiaojiao, Liu Wenjing, Li Yuanqin, Zhao Li, Zhu Shuyang(Department of Respiratory Medicine, the Affiliated Hospital of Xuzhou Medical University, Xuzhou 221000, China)

机构地区：[1]徐州医科大学附属医院呼吸内科,221000

出　　处：《国际呼吸杂志》2018年第21期1609-1615,共7页International Journal of Respiration

基　　金：国家自然科学基金青年基金项目（81600044）;江苏省青年医学人才项目（QNRC2016798）

摘　　要：目的 观察香烟烟雾暴露后,支气管哮喘 （简称哮喘）大鼠肺组织及气道上皮瘦素表达的变化。方法 30只雄性SD大鼠随机分为5组,即正常对照组 （腹腔注射生理盐水1ml）,香烟烟雾对照组 （正常对照组基础上烟熏10支/d连续4周）,哮喘模型组 [腹腔注射鸡卵白蛋白/Al（OH）3混合液1ml致敏],香烟烟雾哮喘组 （在哮喘模型组基础上烟熏10支/d连续4周）,地塞米松处理组（香烟烟雾哮喘组基础上,地塞米松2mg·kg^-1·d^-1腹腔注射1周）,每组6只。收集支气管肺泡灌洗液 （BALF）检测细胞计数及分类,应用 HE染色观察肺组织病理学改变;行 Westernblot法及免疫组织化学染色法分别检测肺组织及气道上皮瘦素蛋白表达水平。酶联免疫吸附测定法检测肺组织白介素17 （IL-17）表达水平。结果 与正常对照组相比,哮喘模型组BALF中白细胞数、中性粒细胞数及气道壁厚度明显升高,而香烟烟雾哮喘组白细胞数、中性粒细胞数和气道壁厚度明显高于哮喘模型组,差异有统计学意义 （F =528.147、380.160、8.771,P 值均〈0.05）;与正常对照组相比,哮喘模型组瘦素及IL-17表达升高,瘦素在气道上皮染色强度增加,而香烟烟雾哮喘组瘦素及IL-17表达明显高于哮喘模型组,差异有统计学意义 （F =5.090、11.497,P 值均〈0.05）;与香烟烟雾哮喘组比较,地塞米松处理组BALF中白细胞数、中性粒细胞数降低,气道重塑改善,肺组织瘦素及IL-17表达降低,瘦素在地塞米松处理组气道上皮染色强度减弱,差异有统计学意义 （F =5.090、11.497,P 值均〈0.05）。结论 香烟烟雾暴露可能通过增加瘦素表达加重气道炎症和气道重塑;哮喘大鼠气道上皮瘦素表达增加,瘦素可能参与了哮喘炎症过程;地塞米松干预可以降低气道上皮瘦素表达,改善气道炎症,提示地塞米松的抗炎机制可能与瘦素有关。Objective To observe the expression of leptin in bronchial epithelium of asthmatic ratsafter cigarette smoke exposure. Methods The 30 experimental rats were randomly divided into five groups, namely, normal control group（intraperitoneal injection of normal saline 1 ml）, cigarette smoke control group （exposure of smoking gas lasted four weeks with 10 cigarettes per day）, asthmatic model group [intraperitoneal injection of ovalbumin/Al（OH）3 mixture 1 ml], cigarette smoke asthmatic group （based on asthmatic model group, exposure of smoking gas lasted four weeks with 10 cigarettes per day）, examethasone intervention group （based on smoke asthmatic group, rats were treated with intraperitoneal injection of dexamethasone 2 mg·kg^-1 · d^-1 lasting one week）, six rats in each group. Bronchoalveolar lavage fluid （BALF） were collected to detect the cell counting and classification. Pathological changes of lungtissue were observed after HE staining. Expressions of leptin was detected by Western blot and immunohistochemistry respectively. We detected the level of IL-17 in lung tissue by the method of enzyme linked immunosorbent assay. Results Compared with normal control group, the number of airway inflammation cells increased in BALF, expressions of leptin increased in lung tissues of groups of cigarette smoke control group, asthmatic model group and cigarette smoke asthmatic group. Compared with cigeratte smoke asthmatic group, the number of airway inflammation cells decreased in BALF, expressions of leptin decreased in lung tissues of groups of dexamethasone intervention group. Airway inflammation attenuated and lung tissue staining intensity reduced in groups of dexamethasone intervention group. Conclusions Cigarette smoke exposure obviously aggravate airway inflammation in asthmatic rats, and dexamethasone effectively alleviate airway inflammation, the mechanism of which may be related to leptin.

关 键 词：哮喘 香烟烟雾 瘦素 地塞米松 

分 类 号：R562.25[医药卫生—呼吸系统]