PM_(2.5)和SO_2复合暴露对大鼠心脏病理学及炎症因子表达的影响  

Effects of PM_(2.5) and SO_2 combined exposure on histopathology and gene expression of inflammatory factors in hearts of rats

作　　者：赵利芳[1] 张书源[2] 佟金龙[1] 闫宇超 徐冲[1] 孟紫强[1] 李瑞金[1] 

机构地区：[1]山西大学环境科学研究所,太原030006 [2]合肥工业大学宣城校区机械工程系,宣城242000

出　　处：《环境科学学报》2017年第5期2006-2011,共6页Acta Scientiae Circumstantiae

基　　金：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-3SO_2组及1.5、6、24 mg·kg^(-1)PM_(2.5)和5.6 mg·m-3SO_2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、i NOS基因表达及NO含量.结果表明,与对照组相比,SO_2(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SO_2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SO_2(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.1.5mg·kg^(-1)PM_(2.5)和SO_2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SO_2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SO_2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SO_2(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SO_2引发心脏疾病的重要机制.Male SD rats were randomly divided into six groups including the control,PM2.5exposure at 1.5 mg·kg^-1 body weight（b.w.）,SO2 exposure at5.6 mg ·m^-3,and the other three double exposure groups of PM2.5at 1.5,6 and 24 mg·kg^-1b.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 I NOS） and NO levels in hearts.The results showed that single exposure of SO2 or PM2.5didn＇ t cause obvious myocardial cell injury.However,double exposure to PM2.5and 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 PM2.5at 1.5mg·kg^-1b.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 I NOS and an increased NO level in rat hearts were observed for double exposure groups of SO2 and PM2.5when compared with the control group.These results suggested that the exposure to PM2.5together with SO2 generated histopathologic damage and high-levels of pro-inflammatory cytokines in rat hearts,which may be one of the important mechanisms of PM2.5plus SO2-triggered heart disease.

关 键 词：PM2.5 SO2 大鼠 心脏 促炎细胞因子 NO 

分 类 号：X171.5[环境科学与工程—环境科学]