上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（基础研究） • 上一篇    下一篇

PM2.5对被动吸烟大鼠慢性气道炎症及氧化应激反应的影响

胡建荣1,2，许华俊1，李庆云1，李春雷3，孙娴雯1，张秀娟1   

  1. 1.上海交通大学 医学院附属瑞金医院呼吸科， 上海 200025； 2.上海交通大学 医学院附属仁济医院嘉定分院呼吸科， 上海 201800； 3.复旦大学环境科学与工程系， 上海 200433
  • 出版日期:2014-05-28 发布日期:2014-05-30
  • 通讯作者: 李庆云, 电子信箱: liqingyun68@hotmail.com。
  • 作者简介:胡建荣（1969—）， 男， 副主任医师， 学士; 电子信箱: 13524500327@163.com。
  • 基金资助:

    上海市科委科技创新计划（10231203902）；上海市嘉定区卫生局科研基金（2013-KY-004）

Effects of short-term exposure to PM2.5on chronic airway inflammation and oxidative stress of passive smoking rats

HU Jian-rong1,2, XU Hua-jun1, LI Qing-yun1, LI Chun-lei3,SUN Xian-wen1, ZHANG Xiu-juan1   

  1. 1.Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; 2.Department of Respiratory Medicine, Renji Hospital Jiading Branch, Shanghai Jiao Tong University School of Medicine, Shanghai 201800, China; 3.Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China
  • Online:2014-05-28 Published:2014-05-30
  • Supported by:

    Innovation Program of Science and Technology Commission of Shanghai Municipality,10231203902; Scientific Research Foundation of Health Bureau of Jiading District of Shanghai, 2013-KY-004

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摘要：

目的 探讨PM2.5短期暴露对被动吸烟大鼠慢性气道炎症和氧化应激反应的影响及可能机制。方法 48只雄性Wistar大鼠分为正常对照组（n=12）和被动吸烟模型组（n= 36），后者在给予被动吸烟45 d后再随机分为单纯被动吸烟组、低剂量（1.25 mg/mL） PM2.5暴露组和高剂量（5 mg/ mL） PM2.5暴露组（n=12）。在末次PM2.5染毒24 h时点，测定大鼠肺功能；收集支气管-肺泡灌洗液（BALF），细胞涂片及吉姆萨（Giemsa）染色后进行细胞计数及分类，对 BALF中白介素-6 （IL-6）、丙二醛（MDA）、总抗氧化能力（T-AOC）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）等指标进行检测；取左肺上叶肺组织，利用光学显微镜（光镜）和透射电子显微镜（透射电镜）观察肺组织学改变和细胞超微结构。结果 单纯被动吸烟组和PM2.5暴露组BALF中白细胞总数均显著高于正常对照组（P<0.05），高剂量PM2.5暴露组中性粒细胞百分比显著高于低剂量PM2.5暴露组（P<0.05）。随着PM2.5暴露浓度的升高，大鼠肺功能参数显著降低（P<0.05）。与正常对照组比较，单纯被动吸烟组和PM2.5暴露组BALF中IL-6和MDA水平显著升高，T-AOC、GSH-Px和CAT水平显著降低，差异均有统计学意义（P<0.05）；与单纯被动吸烟组比较，高剂量PM2.5暴露组IL-6和MDA水平显著升高，T-AOC、GSH-Px和CAT水平显著降低，差异均有统计学意义（P<0.05）。光镜观察可见单纯被动吸烟组大鼠的支气管壁、血管腔及小气道内中性粒细胞、淋巴细胞、巨噬细胞及嗜酸性粒细胞浸润，肺泡间隔明显变薄或融合，肺泡腔内渗出、充血，肺泡管扩张等结构破坏；PM2.5暴露组上述炎症过程进一步加剧，透射电镜观察发现巨噬细胞和肺泡Ⅱ型上皮细胞超微结构发生明显改变。结论 PM2.5短期暴露可加重被动吸烟大鼠气道慢性炎症及氧化应激反应。

关键词: PM2.5, 慢性气道炎症, 氧化应激

Abstract:

Objective To explore the effects of short-term exposure to PM2.5 on the chronic airway inflammation and oxidative stress of passive smoking rats and the possible mechanisms. Methods Forty eight male Wistar rats were randomly divided into the normal control group (n=12) and the passive smoking model group (n=36). Rats of the latter group were then randomly divided into the simple passive smoking group (n=12), low dose (1.25 mg/mL) PM2.5 exposure group (n=12), and high dose (5 mg/ mL) PM2.5 exposure group (n=12) after being given passive smoking for 45 d. The pulmonary function of rats was detected at the time point of 24 h after stopping exposure to PM2.5. The bronchoalveolar lavage fluid (BALF) was collected and cells were counted and classified after being smeared and stained by Giemsa. IL-6, T-AOC, MDA, GSH-Px, and CAT in BALF were measured. The tissues of left lung lobes were excised and the histological changes and intracellular ultrastructure were observed by the optical microscopy and electron microscopy. Results Total cell count of BALF of the passive smoking model group was significantly higher than that of the normal control group (P<0.05). The percentage of neutrophils of high dose PM2.5 exposure group was significantly higher than that of the low dose PM2.5 exposure group (P<0.05). The parameters of pulmonary function of rats were significantly decreased with the increase of the exposure concentration of PM2.5 (P<0.05). Compared to the normal control group, the IL-6 and MDA levels of BALF of the passive smoking model group were significantly increased and the T-AOC, GSH-Px, and CAT levels were significantly decreased. The differences were statistically significant (P<0.05). Compared to the simple passive smoking group, the IL-6 and MDA levels of the high dose PM2.5 exposure group were significantly increased and the T-AOC, GSH-Px, and CAT levels were significantly decreased. The differences were statistically significant (P<0.05). The results of optical microscopy showed that neutrophils, lymphocytes, macrophages, and acidophilic granulocytes in bronchial walls, vessel lumens, and small airways of rats of the passive smoking model group were infiltrated and structural damages were appeared, such as significantly thinned and fused interalveolar septum, effusion and congestion in alveolar spaces, and dilated alveolar ducts. Above inflammatory process of the PM2.5 exposure group was further exacerbated. The electron microscopy showed that the ultrastructure of type Ⅱ had obvious changes. Conclusion Short-term exposure to PM2.5 can aggravate the chronic airway inflammation and oxidative stress of passive smoking rats.

Key words: PM2.5, chronic airway inflammation, oxidative stress