研究报告
张舒婕,李广科,桑楠.NO2吸入诱导小鼠肺组织上皮细胞间质转化及单酰基甘油酯酶抑制的保护作用[J].环境科学学报,2016,36(11):4272-4277
NO2吸入诱导小鼠肺组织上皮细胞间质转化及单酰基甘油酯酶抑制的保护作用
- Monoacylglycerol lipase inhibition prevents NO2-induced epithelial-mesenchymal transitions in lungs of mice
- 基金项目：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）
- 作者
- 单位
- 张舒婕
- 山西大学环境与资源学院, 太原 030006
- 李广科
- 山西大学环境与资源学院, 太原 030006
- 桑楠
- 山西大学环境与资源学院, 太原 030006
- 摘要：通过二氧化氮（NO2）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-184预处理后再次进行小鼠NO2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-184对E-cadherin和α-SMA表达水平的影响.结果表明，NO2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NO2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NO2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，NO2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.
- Abstract：In the present study, we aimed to study the effect of nitrogen dioxide (NO2) 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 NO2 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 NO2. The results indicated that NO2 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-184 decreased the content of PGE2, and inhibited E-cadherin decrease and α-SMA elevation in lungs caused by NO2 inhalation. It was implied that NO2 inhalation caused EMT process, and MAGL inhibition prevented the effects by regulating PGE2 release.
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