Rat lung response to PM2.5 exposure under different cold stresses.

Rat lung response to PM2.5 exposure under different cold stresses.
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不同冷应激下大鼠肺对 PM2.5 暴露的反应。

DOI:
10.3390/ijerph111212915
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发表时间:
2014-12
影响因子:
--
通讯作者:
Niu J
Niu J
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Luo B;Shi H;Wang L;Shi Y;Wang C;Yang J;Wan Y;Niu J

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据报告,环境颗粒物和温度对呼吸道疾病住院和死亡有叠加效应。本研究的目的是通过评估炎症和氧化应激反应来讨论冷应激和细颗粒物(PM2.5)暴露的交互性肺毒性。将48只体重和年龄相匹配的Wistar雄性大鼠随机分为6组,分别进行冷应激(0 °C、10 °C和20 °C(正常对照))和冷应激+PM2.5暴露。单纯冷应激组腹腔内滴注生理盐水0.25 mL,冷应激+PM2.5暴露组腹腔内滴注PM2.5 8 mg/0.25 mL。这些程序进行三次,每次处理间隔48小时。在第三次处理48小时后处死所有大鼠。收集支气管肺泡灌洗液(BALF)用于分析炎性细胞和细胞因子,并测定肺匀浆MDA用于氧化应激的评估。结果显示,PM2.5暴露组BALF中细胞总数和中性粒细胞水平均高于对照组(p < 0.05)。PM2.5暴露组BALF中TNF-α、CRP、IL-6、IL-8水平与冷应激强度呈负相关。仅0 °C冷应激组炎性细胞因子和丙二醛(MDA)含量显著升高,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性显著下降(p < 0.05)。双因素方差分析发现PM2.5暴露与冷应激对中性粒细胞、IL-6、IL-8水平和SOD活性有显著交互作用(p < 0.05)。这些数据表明,炎症和氧化应激参与了PM2. 5暴露和冷应激对肺毒性的累加效应,为环境PM2. 5和冷应激对健康影响的流行病学研究提供了解释。
Ambient particulate matters and temperature were reported to have additive effects over the respiratory disease hospital admissions and deaths. The purpose of this study is to discuss the interactive pulmonary toxicities of cold stress and fine particulate matter (PM2.5) exposure by estimating inflammation and oxidative stress responses. 48 Wistar male rats, matched by weight and age, were randomly assigned to six groups, which were treated with cold stress alone (0 °C, 10 °C, and 20 °C (Normal control)) and cold stresses plus PM2.5 exposures respectively. Cold stress alone groups were intratracheal instillation of 0.25 mL normal saline, while cold stress plus PM2.5 exposure groups were intratracheal instillation of 8 mg/0.25 mL PM2.5. These procedures were carried out for three times with an interval of 48 hours for each treatment. All rats were sacrificed after 48 hours of the third treatment. The bronchoalveolar lavage fluid (BALF) was collected for analyzing inflammatory cells and cytokines, and lung homogenate MDA was determined for oxidative stress estimation. Results showed higher level of total cell and neutrophil in the BALF of PM2.5 exposed groups (p < 0.05). Negative relationships between cold stress intensity and the level of tumor necrosis factor alpha (TNF-a), C-reactive protein (CRP) interleukin-6 (IL-6) and interleukin-8 (IL-8) in BALF were indicated in PM2.5 exposure groups. Exposure to cold stress alone caused significant increase of inflammatory cytokines and methane dicarboxylic aldehyde (MDA) and decline of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity only in 0 °C exposure group (p < 0.05). The two-way ANOVA found significant interactive effects between PM2.5 exposure and cold stress in the level of neutrophil, IL-6 and IL-8 and SOD activity (p < 0.05). These data demonstrated that inflammation and oxidative stress involved in the additive effect of PM2.5 exposure and cold stress on pulmonary toxicity, providing explanation for epidemiological studies on the health effect of ambient PM2.5 and cold stress.
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