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目的研究PM2.5短期暴露对大鼠系统性炎症及主动脉细胞间黏附分子-1(ICAM-1)及血管细胞黏附分子-1(VCAM-1)基因表达的影响,初步探讨PM2.5心血管毒性损伤机制。方法采集空气中PM2.5样本并制备成20 mg/ml的混悬液。24只SD大鼠随机分为对照组、低剂量染毒组和高剂量染毒组,每组8只,分别给予气管内灌注生理盐水或不同浓度混悬液,每日1次,连续染毒7 d。采用ELISA技术检测各组大鼠血清中炎症因子白细胞介素-6(IL-6)和单核细胞趋化蛋白-1(MCP-1)的水平;采用荧光定量PCR技术检测大鼠主动脉VCAM-1、ICAM-1基因表达水平。结果 PM2.5暴露显著增加了血清MCP-1和IL-6水平。对照组、低剂量组和高剂量组血清MCP-1浓度分别为(5.28±0.24)pg/ml、(7.00±0.55)pg/ml和(11.02±1.00)pg/ml(P<0.01);各组血清IL-6浓度分别为(40.17±1.79)pg/ml、(56.08±4.39)pg/ml(P<0.05)和(76.15±4.60)pg/ml(P<0.01)。低剂量组和高剂量组动脉组织ICAM-1 mRNA水平分别为对照组的1.8倍和4.1倍;VCAM-1 mRNA水平分别为对照组的4.0倍和4.6倍。结论暴露于PM2.5可引起大鼠血清炎症因子水平及动脉组织相关黏附分子表达增加,且呈剂量依赖性。诱导系统性炎症可能是PM2.5心血管毒性机制之一。
Objective To investigate the effects of short-term PM2.5 exposure on systemic inflammation and the expression of ICAM-1 and VCAM-1 in rats, Vascular Toxicity Injury Mechanism. Methods PM2.5 air samples were collected and prepared as 20 mg / ml suspension. Twenty-four SD rats were randomly divided into control group, low-dose group and high-dose group, with 8 rats in each group. Rats were given intratracheal instillation of normal saline or different concentrations of suspension once a day for continuous exposure 7 d. The levels of inflammatory cytokines interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) in sera of rats in each group were detected by ELISA. Fluorescent quantitative PCR was used to detect the expression of VCAM -1, ICAM-1 gene expression levels. Results PM2.5 exposure significantly increased serum MCP-1 and IL-6 levels. The concentrations of MCP-1 in the control group, low dose group and high dose group were 5.28 ± 0.24 pg / ml, 7.00 ± 0.55 pg / ml and 11.02 ± 1.00 pg / ml respectively Serum levels of IL-6 were (40.17 ± 1.79) pg / ml, (56.08 ± 4.39) pg / ml (P <0.05) and (76.15 ± 4.60) pg / ml respectively. The levels of ICAM-1 mRNA in arterial tissue of low dose group and high dose group were 1.8 times and 4.1 times that of control group, respectively. The levels of VCAM-1 mRNA were 4.0 times and 4.6 times higher than that of control group respectively. Conclusion Exposure to PM2.5 can induce serum inflammatory cytokines and increase the expression of arterial tissue-associated adhesion molecules in a dose-dependent manner. Induction of systemic inflammation may be one of the mechanisms of PM2.5 cardiovascular toxicity.