药红梅, 吕吉元. PM2.5不同成分致冠状动脉粥样硬化大鼠炎症作用的探讨[J]. 环境与职业医学, 2010, 27(11): 673-676.
引用本文: 药红梅, 吕吉元. PM2.5不同成分致冠状动脉粥样硬化大鼠炎症作用的探讨[J]. 环境与职业医学, 2010, 27(11): 673-676.
YAO Hong-mei , LÜ Ji-yuan . A Study on Inflammation Induced by Different Components of PM2.5 in Coronary Atherosclerosis in Rats[J]. Journal of Environmental and Occupational Medicine, 2010, 27(11): 673-676.
Citation: YAO Hong-mei , LÜ Ji-yuan . A Study on Inflammation Induced by Different Components of PM2.5 in Coronary Atherosclerosis in Rats[J]. Journal of Environmental and Occupational Medicine, 2010, 27(11): 673-676.

PM2.5不同成分致冠状动脉粥样硬化大鼠炎症作用的探讨

A Study on Inflammation Induced by Different Components of PM2.5 in Coronary Atherosclerosis in Rats

  • 摘要: 目的 探讨大气细颗粒物(PM2.5)标准品的水溶性及酸溶性成分对冠状动脉粥样硬化大鼠的致炎作用。

    方法 48只Wistar大鼠随机分为对照组和冠状动脉粥样硬化模型组(模型组),每组各24只。对照组饲喂正常饲料,模型组饲喂高胆固醇饲料,12周后冠脉病理切片示模型成功建立。提取PM2.5的水溶性成分(WSC)及酸溶性成分(ASC)。将对照组和模型组再各自随机分为3组,分别为正常对照组、WSC对照组、ASC对照组;以及模型对照组、WSC模型组、ASC模型组,每组8只。WSC对照组和WSC模型组(均称WSC组)尾静脉注射WSC (40 mg/kg)染毒,ASC对照组和ASC模型组(均称ASC组)尾静脉注射ASC (40 mg/kg)染毒,而正常对照组和模型对照组(均称空白组)则以尾静脉注射生理盐水。染毒24 h后处死大鼠,测定血清中的白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的含量及心肌中的核转录因子-κB (NF-κB)活性。

    结果 WSC组血清TNF-α水平为(2.83& #177;0.97) ng/mL,高于空白组(2.53& #177;0.76) ng/mL;心肌NF-κB活性为(14.56& #177;10.58)%,高于空白组(7.33& #177;3.97)%。ASC组心肌NF-κB活性为(18.80& #177;17.04)﹪,也高于空白组。冠状动脉粥样硬化模型在升高IL-6、激活心肌NF-κB方面,与WSC、ASC分别存在协同作用。

    结论 WSC具有升高TNF-α水平、激活心肌NF-κB活性的作用;ASC也具有激活心肌NF-κB活性的作用。冠状动脉粥样硬化模型还与WSC、ASC染毒具有交互作用,主要表现在升高IL-6水平,激活心肌NF-κB活性的作用上,表明PM2.5水溶性成分及酸溶性成分均可致冠状动脉粥样硬化大鼠的炎症作用。

     

    Abstract: Objective To understand inflammation induced by the water-soluble and acid-soluble components of PM2.5 in rats having coronary atherosclerosis.

    Methods Total of 48 Wistar rats were randomly divided into control group and coronary atherosclerotic model group (model group) (n=24). The control group was fed normal diet, and the model group was fed highcholesterol diet. 12 weeks later, coronary atherosclerosis in model group was confirmed pathological biopsy. The water-soluble components (WSC)and acid-soluble components (ASC)of PM2.5 were extracted. The control group and model group were further divided into 3 groups respectively. They were the normal control group, WSC control group, ASC control group, model control group, WSC model group, and ASC model group (n=8 each group). WSC control group and WSC model group (collectively called WSC group)were injected with WSC (40 mg/kg); ASC control group and ASC model group (collectively called ASC group)were injected with ASC (40 mg/kg); the normal control group and model control group (collectively called blank group)were injected with normal saline (NS). The rats were killed after 24 h of exposure. IL-6/TNF-α in serum and NF-κB in myocardial were measured.

    Results The TNF-α in WSC group (2.83& #177;0.97)ng/mL was higher than the blank group (2.53& #177;0.76)ng/mL; the myocardial NF-κB activation level in WSC group (14.56& #177;10.58)% was higher than the blank group (7.33& #177;3.97)%. The myocardial NF-κB activation in the ASC group (18.80& #177;17.04)% was higher than the blank group (7.33& #177;3.97)%. Model of coronary atherosclerosis showed a synergistic effect on the WSC and ASC in increasing IL-6 and activating of myocardial NF-κB.

    Conclusion WSC may increase TNF-α, and activate myocardial NF-κB; ASC may activate myocardial NF-κB. Coronary atherosclerosis model suggested an interaction among WSC and ASC in increasing IL-6 and activating NF-κB. The acid-soluble and water-soluble components of PM2.5 could contribute to the inflammation in coronary atherosclerosis in rats.

     

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