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丁世彬,高丽云,李玉春,卜勇军,张国富.慢性PM2. 5 暴露对C57BL/ 6J 小鼠肺组织炎症和NLRP3 炎性小体活性的影响[J].中国实验动物学报,2019,27(4):444~449.
慢性PM2. 5 暴露对C57BL/ 6J 小鼠肺组织炎症和NLRP3 炎性小体活性的影响
Effects of chronic PM2. 5 exposure on lung inflammation and NLRP3 inflammasome activation in C57BL / 6J mice
投稿时间:2019-02-21  
DOI:10. 3969 / j.issn.1005-4847. 2019. 04. 004
中文关键词:  小鼠  PM2. 5  NLRP3 炎性小体  肺炎症
英文关键词:mouse  PM2. 5  NLRP3 inflammasome  lung inflammation
基金项目:
作者单位E-mail
丁世彬 1. 新乡医学院,河南新乡 453003
2. 河南省分子诊断与检验医学协同创新中心,新乡 453003 
dingshibin@ 163.com 
高丽云 新乡医学院,河南新乡 453003  
李玉春 新乡医学院,河南新乡 453003  
卜勇军 新乡医学院,河南新乡 453003  
张国富 新乡医学院,河南新乡 453003  
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中文摘要:
      目的 研究慢性PM2. 5 暴露对小鼠肺炎症和NLRP3 炎性小体活性的影响,为防治PM2. 5 所致肺损伤提供新靶点。方法 雄性C57BL/6J 小鼠通过不同剂量气管滴注法进行PM2. 5 染毒,剂量为2, 10 mg/ (kg?bw),对照组小鼠滴注生理盐水。小鼠连续滴注20 次,每3 d 染毒1 次后,取血和肺组织。三组小鼠进行血细胞计数;用免疫荧光染色法检测肺组织巨噬细胞水平;用试剂盒测定肺组织中白细胞介素(interleukin,IL)-1β,IL-18 水平及caspase-1 活性;用实时定量PCR 法检测肺组织NLRP3 炎性小体相关mRNA 表达水平。结果 两个剂量PM2. 5 染毒均能明显降低单核细胞百分比( P < 0. 01),增加中性粒白细胞百分比( P < 0. 01);导致肺炎症发生;增加肺组织caspase-1 活性( P < 0. 01)及NLRP3 和ASC 的mRNA 表达( P < 0. 01)。与对照组相比,两个剂量组小鼠肺组织IL-1β 和IL-18 水平均显著增高( P < 0. 01)。结论 慢性PM2. 5 暴露可能通过激活肺组织NLRP3 炎性小体导致肺炎症发生。
英文摘要:
      Objective  To study the effects of chronic PM2. 5 exposure on lung inflammation and NLRP3inflammasome activation in mice, and to provide a new target for prevention and treatment of lung injury caused by PM2. 5.Methods Male C57BL/6J mice were exposed to two doses of PM2. 5 by tracheal instillation [2, 10 mg/ (kg.bw)], andthe control mice were instilled with normal saline. After mice had been instilled for 20 times (1 time every 3 days), bloodand lung tissues were collected. Blood cells were counted, and lung tissue macrophage levels were measured usingimmunofluorescence staining. Interleukin (IL)-1β and IL-18 levels and caspase-1 activity in lung tissues were determinedusing ELISA and caspase-1 activity measurement kits. The expression levels of NLRP3 inflammasome-associated mRNA inlung tissue were detected using real-time PCR. Results The two doses of PM2. 5 significantly reduced the percentage ofmonocytes ( P < 0. 01) and induced lung inflammation. The PM2. 5-treated mice had a higher percentage of neutrophils ( P < 0. 01), a higher in caspase-1 activity ( P < 0. 01), and a higher in mRNA expression of NLRP3 and ASC ( P < 0. 01) inlung tissues compared with the control mice. IL-1β and IL-18 levels in the lung tissues of the two PM2. 5-exposed groupswere significantly higher than those seen in the control group (both P < 0. 01). Conclusion Chronic PM2. 5 exposure may induce lung inflammation by activating the NLRP3 inflammasome in the lung tissue.
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