RCAN1抑制小鼠腹腔巨噬细胞NLRP3炎性体的活化  

RCAN1 inhibits NLRP3 inflammasome activation in murine peritoneal macrophages

作　　者：雷倩倩[1] 于水星 李宁[1] 胡桂秋[1] 韩文瑜[1] 杜崇涛[1] 陈巍[1] 杨勇军[1] 

机构地区：[1]吉林大学动物医学学院,吉林长春130062

出　　处：《畜牧与兽医》2016年第1期39-43,共5页Animal Husbandry & Veterinary Medicine

基　　金：国家自然科学基金资助项目(31172298)

摘　　要：为探讨RCAN1对NLRP3炎性体活化的影响,分离培养了野生型小鼠和RCAN1基因缺失小鼠的腹腔巨噬细胞,应用LPS联合ATP处理细胞,分别收集细胞培养上清和细胞裂解液。采用Western blot和ELISA方法,分别检测IL-1β、caspase-1的剪切成熟以及IL-1β和TNF-α的分泌。结果显示:相比来源于野生型小鼠的腹腔巨噬细胞,RCAN1基因缺失能够显著促进ATP介导的caspase-1的剪切成熟和IL-1β的分泌,而不影响TNF-α的分泌。以上结果表明,RCAN1能够负向调控NLRP3炎性体活化信号,抑制IL-1β的分泌。To investigate the effect of RCAN1 on the activation of NLRP3,in this study,we isolated and cultured the peritoneal macrophages from wild type and RCAN1 deficient mice. Cell culture supernatant and lysate were collected after cells were treated by LPS combined with ATP. Western blot and ELISA method were used to detect the expression of IL- 1β and caspase- 1,and the secretion of IL- 1β and TNF- α,respectively. The results showed that the deletion of RCAN1 gene could significantly promote the expression of caspase- 1 mediated by ATP and the secretion of IL- 1β,but not affect the secretion of TNF- α. The findings demonstrate that RCAN1 can negatively regulate the activation of NLRP3 and inhibit the secretion of IL- 1β.

关 键 词：RCAN1 NLRP3 腹腔巨噬细胞 

分 类 号：S852.4[农业科学—基础兽医学]