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研究报告

赵利芳,张书源,佟金龙,闫宇超,徐冲,孟紫强,李瑞金.PM_2.5和SO₂复合暴露对大鼠心脏病理学及炎症因子表达的影响[J].环境科学学报,2017,37(5):2006-2011

Effects of PM_2.5 and SO₂ combined exposure on histopathology and gene expression of inflammatory factors in hearts of rats

基金项目：山西省自然科学基金（No.2014011036-2）；山西省高等学校科技创新项目（No.2014110）；山西省回国留学人员科研项目（No.2013-16）

摘要：将雄性SD大鼠分为对照组、1.5 mg·kg^-1 PM_2.5组、5.6 mg·m^-3 SO₂组及1.5、6、24 mg·kg^-1 PM_2.5和5.6 mg·m^-3 SO₂联合作用组.采用HE染色法、荧光实时定量PCR和ELISA等方法测定各组大鼠心脏组织病理学变化和炎症因子IL-1β、IL-6、TNF-α、iNOS基因表达及NO含量.结果表明，与对照组相比，SO₂（5.6 mg·m^-3）或PM_2.5（1.5 mg·kg^-1）单独作用没有引起明显的心肌细胞损伤，而PM_2.5和SO₂共同作用导致不同程度的心肌排列紊乱，细胞间隙增大及炎症细胞浸润和出血，比SO₂（5.6 mg·m^-3）或PM_2.5（1.5 mg·kg^-1）单独作用有严重的病理学损伤.1.5 mg·kg^-1 PM_2.5和SO₂引起4个基因表达和NO水平的变化与对照组相比没有统计学意义，而PM_2.5和SO₂联合处理引起大鼠心脏炎症因子表达水平比对照组显著增高，同时与SO₂组或PM_2.5组相比也有显著升高.提示在本实验条件下，相比于PM_2.5（1.5 mg·kg^-1）和SO₂（5.6 mg·m^-3）单独作用，二者复合暴露能引起心脏组织病理损伤和炎症因子高表达，这可能是PM_2.5和SO₂引发心脏疾病的重要机制.

Abstract：Male SD rats were randomly divided into six groups including the control, PM_2.5 exposure at 1.5 mg·kg^-1 body weight (b.w.), SO₂ exposure at 5.6 mg·m^-3, and the other three double exposure groups of PM_2.5 at 1.5, 6 and 24 mg·kg^-1 b.w. and SO₂ exposure at 5.6 mg·m^-3. The HE staining, real-time RT-PCR and ELISA were used to detect the histopathologic change, mRNA and protein levels of inflammatory genes (IL-1β, IL-6, TNF-α and iNOS) and NO levels in hearts. The results showed that single exposure of SO₂ or PM_2.5 didn't cause obvious myocardial cell injury. However, double exposure to PM_2.5 and SO₂ induced more severe pathological changes, such as myocardial disarray, inflammatory cell infiltration, increased myocardial cell spacing and hyperemia. There were no significant differences in 4 gene expressions, and NO levels in rats between single exposure of PM_2.5 at 1.5 mg·kg^-1 b.w. or SO₂ exposure at 5.6 mg·m^-3 and the control group. However, a significantly enhanced high-expression of IL-1β, IL-6, TNF-α and iNOS and an increased NO level in rat hearts were observed for double exposure groups of SO₂ and PM_2.5 when compared with the control group. These results suggested that the exposure to PM_2.5 together with SO₂ generated histopathologic damage and high-levels of pro-inflammatory cytokines in rat hearts, which may be one of the important mechanisms of PM_2.5 plus SO₂-triggered heart disease.