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曲红梅, 牛静萍, 魁发瑞, 邵国军. 大气中PM2.5致大鼠呼吸道急性损伤作用[J]. 中国公共卫生, 2006, 22(5): 598-599. DOI: 10.11847/zgggws2006-22-05-56
引用本文: 曲红梅, 牛静萍, 魁发瑞, 邵国军. 大气中PM2.5致大鼠呼吸道急性损伤作用[J]. 中国公共卫生, 2006, 22(5): 598-599. DOI: 10.11847/zgggws2006-22-05-56
QU Hongmei, NIU Jingping, KUI Farui, . Study on rat pulmonary toxicity induced by PM2.5 in atmosphere of Lanzhou city[J]. Chinese Journal of Public Health, 2006, 22(5): 598-599. DOI: 10.11847/zgggws2006-22-05-56
Citation: QU Hongmei, NIU Jingping, KUI Farui, . Study on rat pulmonary toxicity induced by PM2.5 in atmosphere of Lanzhou city[J]. Chinese Journal of Public Health, 2006, 22(5): 598-599. DOI: 10.11847/zgggws2006-22-05-56

大气中PM2.5致大鼠呼吸道急性损伤作用

Study on rat pulmonary toxicity induced by PM2.5 in atmosphere of Lanzhou city

  • 摘要:
      目的   探讨大气中细颗粒物(PM2.5)致大鼠呼吸道的急性损伤及其机制。
      方法   将体重180~220 g的30只大鼠随机分为5组, 即空白对照组、生理盐水组、高、中、低PM2.53个剂量组进行染毒, 采用气管注入法, 灌注体积0.5 ml, 灌注后第12 d处死大鼠, 进行肺泡灌洗液(BALF)中酸性磷酸酶(ACP)、碱性磷酸酶(AKP)、乳酸脱氢酶(LDH)、白蛋白(ALB)和IgG、IgA测定, 并观察其肺组织病理变化。
      结果   空白对照组和生理盐水组3种酶和蛋白及IgGI、gA差异无统计学意义(P > 0.05), 而其他3个剂量组和生理盐水组差异有统计学意义(P < 0.05)。肺组织病理切片有炎性改变, 单核细胞和中性粒细胞浸润和淋巴细胞增生, 3个实验组随剂量增加肺组织炎性病变程度加重。
      结论   PM2.5可致肺组织细胞和生物膜的损伤, 且引起体液免疫应答和局部粘膜免疫。

     

    Abstract:
      Objective   To study acute injury and mechanism of rats respiratory tract induced by PM2.5.
      Methods   Wistar rats weighing between 180~220 g were randolmly divided into five groups including blank control group, saline control group, three level PM2.5(high, middle and low)groups.Three level PM2.5 groups were instilled intratracheally with 0.5 ml suspensions of PM2.5 and saline control group were instilled intratracheally with 0.5 ml saline.After 12 days rats were killed, pulmonary pathological injury and bronchoalveolar lavage flluid(BALF)of all rats were later examined, including the level of lactate dehy drogenase(LDH), alkaline phosphatase(AKP), acidic phosphatase(ACP), albumin(ALB), immunoglobuli G(IgG), immunoglobuli A(IgA).
      Results   The amount of LDH, AKP, ACP, ALB, IgG, IgA in exposed groups were significantly higher than those in saline control, but no evident difference between blank control and saline control(P < 0.05).Inflammatory changes including neutrophil and monocyte, lymphocyte hyperplasia were observed on pulmonary pathological slide in a dose denpendent way.
      Conclusion   PM2.5 have acute toxic effects on rat pulmonary cells and membrane tissues, also bring sapimmune response and macosal immune response.

     

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