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巨英超, 刘亮, 贺宇彤, 单保恩. 大气细颗粒物PM2.5致Wistar大鼠肺部病变的研究[J]. 肿瘤防治研究, 2017, 44(10): 652-658. DOI: 10.3971/j.issn.1000-8578.2017.17.0272
引用本文: 巨英超, 刘亮, 贺宇彤, 单保恩. 大气细颗粒物PM2.5致Wistar大鼠肺部病变的研究[J]. 肿瘤防治研究, 2017, 44(10): 652-658. DOI: 10.3971/j.issn.1000-8578.2017.17.0272
JU Yingchao, LIU Liang, HE Yutong, SHAN Baoen. Pulmonary Lesions of Wistar Rats Induced by Atmospheric Particulate PM2.5[J]. Cancer Research on Prevention and Treatment, 2017, 44(10): 652-658. DOI: 10.3971/j.issn.1000-8578.2017.17.0272
Citation: JU Yingchao, LIU Liang, HE Yutong, SHAN Baoen. Pulmonary Lesions of Wistar Rats Induced by Atmospheric Particulate PM2.5[J]. Cancer Research on Prevention and Treatment, 2017, 44(10): 652-658. DOI: 10.3971/j.issn.1000-8578.2017.17.0272

大气细颗粒物PM2.5致Wistar大鼠肺部病变的研究

Pulmonary Lesions of Wistar Rats Induced by Atmospheric Particulate PM2.5

  • 摘要:
    目的 探讨大气细颗粒物(particulate matter,PM)PM2.5致肺部病变机制。
    方法 采用实时PM2.5采集器进行PM2.5收集,Wistar大鼠饲养于PM2.5的全身暴露染毒系统,Wistar大鼠每日染毒4小时,共染毒9月,设立实验组及对照组;观察肺组织大体结构及HE染色观察;流式细胞术检测Wistar大鼠T细胞免疫功能、肺组织细胞凋亡、细胞周期及DNA指数;ELISA实验检测Wistar大鼠血清及肺灌洗液中CEA、CA125及SccAg表达水平。
    结果 实验组肺组织以支气管向外周辐射状颜色发暗、偏黑,多处可见白色斑点和泡状凸起,边缘不规则白色隆起;HE染色结果,实验组肺组织纤维化,肺实变严重,肺泡充血,见大量炎性反应增生;实验组CD4/CD8比值显著高于对照组(P < 0.05),血清及肺灌洗液中CA125的表达显著高于对照组(P < 0.05),实验组肺组织细胞凋亡率显著低于对照组,而DNA指数显著增高(均P < 0.05)。
    结论 长期接触PM2.5会造成肺组织出现不同程度结节,肺组织出现大范围炎性反应病变。

     

    Abstract:
    Objective To investigate the mechanism of lung lesions caused by fine particulate matter PM2.5.
    Methods Real-time PM2.5 collector was used to collect PM2.5. Wistar rats were fed on the systemic exposure system of PM2.5. Wistar rats were exposed to 4 hours daily for 9 months. PM2.5 experimental group and control group were set up. General structure of lung tissue and HE staining result were observed. T cell immune function, lung cell apoptosis, cell cycle and DNA index in Wistar rats were detected by flow cytometry. The expression levels of CEA, CA125 and SccAg in serum and lung lavage fluid of Wistar rats were detected by ELISA.
    Results Lung tissues of experimental group were radiated from the periphery of the bronchus with dark, visible white spots and bubble like protrusions with irregular white ridges. HE staining results showed that lung tissues of experimental group were fibrotic, severe consolidation of lung, alveolar hyperemia and massive inflammaroty reactive hyperplasia. CD4/CD8 ratio in experimental group was significantly higher than that in control group(P < 0.05). The expression of CA125 in serum and lung lavage fluid was significantly higher than that in control group(P < 0.05). The apoptosis rate of lung tissues in experimental group was significantly lower than that in control group, but DNA index was significantly higher (P < 0.05).
    Conclusion Long-term exposure to PM2.5 results in different degrees of nodules and a large range of inflammatory reaction in lung tissues.

     

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