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*

doi:10.12047/j.cjap.5788.2019.061

摘要/Abstract

摘要： 目的:探讨维生素E改善暴露于高温与PM_2.5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PM_2.5(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PM_2.5暴露使COPD大鼠肺功能降低(P＜0.05),各PM_2.5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PM_2.5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PM_2.5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, PM_2.5, 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 PM_2.5. 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 PM_2.5 (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 PM_2.5 could inhibit the lung function of COPD rats significantly (P＜0.05); the level of MCP-1 was increased significantly in PM_2.5-exposure groups (P＜0.05); iNOS was increased significantly in the groups of high temperature (P＜0.05). Compared with the single-PM_2.5 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 PM_2.5 could aggravate the inflammation of COPD rats. As an antioxidant, vitamin E may protect the lung from the damage effects.

Key words: high temperature, PM_2.5, vitamin E, chronic obstructive pulmonary disease, rats

刘江涛, 罗斌, 贺小桃, 李兰玉, 徐生刚. 维生素E对暴露于高温及PM_2.5中COPD大鼠呼吸系统的保护性作用^*[J]. 中国应用生理学杂志, 2019, 35(4): 293-296.

LIU Jiang-tao, LUO Bin, HE Xiao-tao, LI Lan-yu, XU Sheng-gang. The protective effects of vitamin E on lung injury caused by high temperature and PM_2.5 in COPD rats[J]. CJAP, 2019, 35(4): 293-296.

参考文献

[1] 申永春, 文富强, 贺蓓. 慢性阻塞性肺疾病全球创议(2011年修订版)概述[J] . 中华医学杂志, 2012, 92(14): 937-938.
[2] Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030[J] . PLoS Med, 2006, 3(11): e442.
[3] Luo B, Liu J, Fei G, et al. Impact of probable interaction of low temperature and ambient fine particulate matter on the function of rats alveolar macrophages[J] . Environ Toxicol Pharmacol, 2017, 49: 172-178.
[4] 罗斌, 刘江涛, 费高强, 等. 不同温度刺激与大气PM2.5对大鼠肺泡巨噬细胞的交互毒性作用研究[J] . 中国应用生理学杂志, 2017, 33(1): 71-75.
[5] Luo B, Shi H, Wang L, et al. Rat lung response to PM2.5 exposure under different cold stresses[J] . Int J Environ Res Public Health, 2014, 11(12): 12915-12926.
[6] Wu S, Ni Y, Li H, et al. Short-term exposure to high ambient air pollution increases airway inflammation and respiratory symptoms in chronic obstructive pulmonary disease patients in Beijing, China[J] . Environ Int, 2016, 94: 76-82.
[7] 张凯, 费高强, 李兴杰, 等. 高温及低温时大气PM_(2.5)对大鼠肺泡巨噬细胞的毒性作用[J] . 环境与健康杂志, 2017, 34(5): 394-397.
[8] Azzi A, Boscoboinik D, Clement S, et al. Vitamin E mediated response of smooth muscle cell to oxidant stress[J] . Diabetes Res Clin Pract, 1999, 45(2-3): 191-198.
[9] Cheng CH, Guo ZX, Wang AL. Growth performance and protective effect of vitamin E on oxidative stress pufferfish (Takifugu obscurus) following by ammonia stress[J] . Fish Physiol Biochem, 2018, 44(2): 735-745.
[10] 王新, 聂燕, 陈红, 等. 兰州城区大气PM_(2.5)污染特征及来源解析[J] . 环境科学, 2016, 37(5): 1619-1628.
[11] Kozma Rde L, Alves EM, Barbosa-de-Oliveira VA, et al. A new experimental model of cigarette smoke-induced emphysema in Wistar rats[J] . J Bras Pneumol, 2014, 40(1): 46-54.
[12] Chen K, Wolf K, Breitner S, et al. Two-way effect modifications of air pollution and air temperature on total natural and cardiovascular mortality in eight European urban areas[J] . Environ Int, 2018, 116: 186-196.
[13] Tian L, Liang F, Guo Q, et al. The effects of interaction between particulate matter and temperature on mortality in Beijing, China[J] . Environ Sci Process Impacts, 2018, 20(2): 395-405.
[14] Ding PH, Wang GS, Guo YL, et al. Urban air pollution and meteorological factors affect emergency department visits of elderly patients with chronic obstructive pulmonary disease in Taiwan[J] . Environ Pollut, 2017, 224: 751-758.
[15] 鲍中未, 郭金兰. 血清白介素-18、单核细胞趋化蛋白-1和高敏C反应蛋白在慢性阻塞性肺疾病检测中的意义[J] . 中外医学研究, 2017, 15(2): 8-11.
[16] 李海凤, 陈静. 肿瘤坏死因子-α诱导核转录因子-κB信号通路在肺纤维化分子机制中作用[J] . 中国职业医学, 2012, 39(5): 442-444.
[17] 高文蔚, 刘敏, 赵博, 等. ICAM-1和iNOS在乌司他丁对呼吸机致大鼠急性肺损伤中的变化[J] . 广东医学, 2016, 37(22): 3367-3368.
[18] 陈业文, 胡元灏, 程龙, 等. 过敏症状儿童室内PM_(2.5)对小鼠巨噬细胞的氧化损伤及VE的抗氧化保护作用研究[J] . 生态毒理学报, 2018, 13(2): 120-127.
[19] 杜喜浩, 蒋硕, 薄亮, 等. 维生素E和ω-3脂肪酸对大气PM_(2.5)心肺损伤的干预研究[J] . 卫生研究, 2017, 46(4): 517-526.
[20] 田程远, 严明, 张云, 等. 杭州市中心城区大气PM2.5暴露致大鼠肺部损伤作用研究[J] . 中国应用生理学杂志, 2018, 34(4): 299-303.