摘要
通过二氧化氮(NO_2)动式吸入染毒模型,探讨其对小鼠肺组织上皮细胞间质转化(epithelial-mesenchymal transitions,EMT)的影响及单酰基甘油酯酶(MAGL)抑制在此过程中的保护作用.首先检测暴露后肺组织硝酸盐、亚硝酸盐的含量,并考察对EMT标志蛋白E-钙粘蛋白(E-cadherin)和α平滑肌肌动蛋白(α-SMA)表达水平的影响.其次,在MAGL抑制剂JZL^(-1)84预处理后再次进行小鼠NO_2动态吸入染毒,检测不同处理条件下前列腺素E2(PGE2)含量,并考察JZL^(-1)84对E-cadherin和α-SMA表达水平的影响.结果表明,NO_2吸入显著上调小鼠肺组织中硝酸盐和亚硝酸盐的含量,且使小鼠肺组织中E-cadherin表达明显降低,α-SMA表达显著升高,说明NO_2通过其体内代谢衍生物可诱导小鼠肺组织EMT发生.而MAGL抑制可显著降低NO_2诱导的小鼠肺组织中前列腺素E2(PGE2)含量升高,并缓解吸入暴露造成的E-cadherin表达下降和α-SMA表达量增加,抑制EMT过程.由此提示,NO_2吸入暴露可诱导小鼠肺组织EMT发生,而MAGL抑制通过调控PGE2水平对这一损伤效应具有保护作用.
In the present study,we aimed to study the effect of nitrogen dioxide（ NO_2） on the epithelial-mesenchymal transitions（ EMT） in lungs mice,and investigated the potential protection of monoacylglycerol lipase（ MAGL） inhibition on the effects. First,we set up an NO_2 exposure model of mice,detected the content of nitrate and nitrite in lungs,and determined the expression of EMT marker proteins,mainly E-cadherin and α-SMA. Afterwards,we pretreated the mice by MAGL disruption,and exposed them to NO_2. The results indicated that NO_2 inhalation elevated the contents of nitrate and nitrite,and activated EMT by significantly increasing the expression of α-SMA and decreasing the expression of E-cadherin in lungs. MAGL inhibition by injecting JZL^（-1）84 decreased the content of PGE2,and inhibited E-cadherin decrease and α-SMA elevation in lungs caused by NO_2 inhalation. It was implied that NO_2 inhalation caused EMT process,and MAGL inhibition prevented the effects by regulating PGE2 release.
出处
《环境科学学报》
CAS
CSCD
北大核心
2016年第11期4272-4277,共6页
Acta Scientiae Circumstantiae
基金
国家自然科学基金(No.21477070)
山西省回国留学人员科研资助项目(No.2015-006)~~
