文章摘要
李小燕,孙 浩,李晓波,陈 瑞.纳米级炭黑颗粒通过激活NLRP3炎性小体诱导小鼠急性肺炎反应[J].南京医科大学学报,2019,(5):643~647
纳米级炭黑颗粒通过激活NLRP3炎性小体诱导小鼠急性肺炎反应
Activation of NLRP3 inflammasome contributes to carbon black nanoparticles⁃induced pulmonary inflammation
投稿时间:2019-02-19  
DOI:10.7655/NYDXBNS20190503
中文关键词: NLRP3炎症小体  纳米炭黑颗粒  IL⁃1β  急性肺炎
英文关键词: NLRP3 inflammasome  CBNPs  IL⁃1β  acute pulmonary inflammation
基金项目:国家自然科学基金重点项目(81730088);国家自然科学基金重大研究计划(91643109)
作者单位
李小燕 东南大学环境医学工程教育部重点实验室江苏 南京 210009 
孙 浩 东南大学环境医学工程教育部重点实验室江苏 南京 210009 
李晓波 东南大学环境医学工程教育部重点实验室江苏 南京 210009 
陈 瑞 东南大学环境医学工程教育部重点实验室江苏 南京 210009 
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中文摘要:
      目的:探讨NLRP3炎性小体在纳米级炭黑颗粒致急性肺炎中的作用。方法:采用动物全身动态暴露系统建立C57BL/6小鼠低剂量分别连续动态吸入纳米级炭黑颗粒3 d及7 d模型,利用ELISA法检测血清及肺泡灌洗液中白细胞介素?1β(interleukin?1β,IL?1β)含量,并收集小鼠全血,行血常规检查。小鼠处死后解剖,通过HE法检测小鼠肺组织病理损伤情况,通过免疫组织化学染色法检测小鼠肺组织NLRP3蛋白表达,之后利用NLRP3基因敲除小鼠做进一步验证。结果:HE染色结果表明,短期暴露于纳米级炭黑颗粒,小鼠出现急性肺部炎症,主要表现为肺泡间隔增宽、炎性细胞浸润,且暴露组与对照组相比病理评分差异具有统计学意义,免疫组化结果表明,暴露组NLRP3阳性细胞数明显多于对照组,暴露组肺泡灌洗液中IL?1β水平明显高于对照组。结论:NLRP3炎性小体的激活参与了纳米级炭黑颗粒短期暴露引起的小鼠急性肺炎。
英文摘要:
      Objective:To investigate the role NLRP3 inflammasome in acute pulmonary inflammation induced by carbon black nanoparticles(CBNPs). Methods:C57BL/6 mice were exposed to carbon black nanoparticles for 3 days and 7 days,respectively. IL?1β levels in serum and BAL fluid were detected by ELISA,and whole blood of mice was collected for routine blood test. The pathological damage of lung tissues was detected by H&E staining,and the expression of NLRP3 protein in lung tissues was detected by immunohistochemical(IHC)staining. Then,all the experiments were repeated in NLRP3 knock out mice and wild type mice. Results:HE staining showed that acute pulmonary inflammation including enlarged alveolar septum and infiltrations of inflammatory cells were observed in mice after short?term carbon black nanoparticles exposure. There were significant differences in pathological scores between the exposure group and the control group. IHC staining results showed that the expression level of NLRP3 in mice exposed to CBNPs was significantly higher than control. The level of IL?1β in BALF and serum of mice exposed to CBNPs were significantly higher than control. Conclusion:NLRP3/caspase?1 signaling pathway contributes to pulmonary inflammation induced by CBNPs short?term exposure.
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