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中国应用生理学杂志 ›› 2019, Vol. 35 ›› Issue (4): 293-296.doi: 10.12047/j.cjap.5788.2019.061

• 研究论文 • 上一篇    下一篇

维生素E对暴露于高温及PM2.5中COPD大鼠呼吸系统的保护性作用*

刘江涛1, 罗斌1, 贺小桃1, 李兰玉1, 徐生刚2△   

  1. 1. 兰州大学公共卫生学院劳动卫生与环境卫生学研究所, 甘肃 兰州 730000;
    2. 河西学院医学院, 甘肃 张掖 734000
  • 收稿日期:2018-11-23 出版日期:2019-07-28 发布日期:2019-11-06
  • 通讯作者: ,Tel: 15002603091; E-mail: 45196808@qq.com
  • 基金资助:
    *河西学院青年基金(QN2016015)

The protective effects of vitamin E on lung injury caused by high temperature and PM2.5 in COPD rats

LIU Jiang-tao1, LUO Bin1, HE Xiao-tao1, LI Lan-yu1, XU Sheng-gang2△   

  1. 1. Institute of Occupational Health and Environmental Health, School of Public Health, Lanzhou University, Lanzhou 730000;
    2. Medical College of Hexi University, Zhangye 734000, China
  • Received:2018-11-23 Online:2019-07-28 Published:2019-11-06

摘要: 目的:探讨维生素E改善暴露于高温与PM2.5对慢性阻塞性肺疾病(COPD)大鼠呼吸系统功能损伤的作用。方法:将54只7周龄SPF级雄性Wistar大鼠随机分成9个实验组(n=6),利用烟草烟雾和气管内滴注脂多糖建立COPD大鼠模型,而后对其进行PM2.5(0 mg/ml、3.2 mg/ml)气管滴注染毒和维生素E腹腔注射(20 mg/ml)干预,随后高温组进行高温(40℃)暴露,每天一次(8 h),持续3 d。末次暴露后检测肺功能,HE染色制作肺组织病理切片,采用试剂盒测定大鼠肺组织中诱导性一氧化氮合酶(iNOS)、肿瘤坏死因子(TNF-α)、单核细胞趋化蛋白1(MCP-1)的表达水平。结果:与对照组相比,高温和PM2.5暴露使COPD大鼠肺功能降低(P<0.05),各PM2.5染毒组中MCP-1含量均有显著升高(P<0.05),高温组中iNOS活性显著增高(P<0.05);与单纯PM2.5染毒组相比,在常温健康和高温COPD维生素E干预组的TNF-α含量均显著降低(P<0.05),三组维生素干预组中MCP-1含量均显著降低(P<0.05),高温COPD维生素干预组中iNOS活性显著降低(P<0.05)。结论:高温与PM2.5可引起并进一步加重COPD大鼠的炎症反应,维生素E作为一种抗氧化剂,可明显改善上述损伤作用,从而保护机体。

关键词: 高温, PM2.5, 维生素E, 慢性阻塞性肺疾病, 大鼠

Abstract: Objective: To investigate the effects of vitamin E on the respiratory function impairment in rats with chronic obstructive pulmonary disease (COPD) after exposed to high temperature and PM2.5. Methods: Fifty-four 7-week-old SPF male Wistar rats were randomly divided into 9 experimental groups (n=6). The rat COPD model was established by lipopolysaccharide (LPS) and smoke exposure. After modeled, the rats were tracheal instilled with PM2.5 (0 mg/ml, 3.2 mg/ml) and intraperitoneally injected with vitamin E at the dose of 40 mg/kg (20 mg/ml). Part of rats (high temperature groups) were then exposed to high temperature (40℃), once (8 h) a day for three consecutive days. After the last exposure, the lung function of rats was detected. The expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) were detected by corresponding ELISA kits. Results: Compared with the control group, exposure of high temperature and PM2.5 could inhibit the lung function of COPD rats significantly (P<0.05); the level of MCP-1 was increased significantly in PM2.5-exposure groups (P<0.05); iNOS was increased significantly in the groups of high temperature (P<0.05). Compared with the single-PM2.5 exposure groups, TNF-α in lung was decreased in the normal temperature health group and high temperature COPD group (P<0.05) after treated with vitamin E; MCP-1 was decreased in all vitamin E-treated groups (P<0.05); the decreased iNOS only appeared in the group of high temperature with vitamin E treatment. Conclusion: High temperature and PM2.5 could aggravate the inflammation of COPD rats. As an antioxidant, vitamin E may protect the lung from the damage effects.

Key words: high temperature, PM2.5, vitamin E, chronic obstructive pulmonary disease, rats

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