肝X受体激动剂抑制NLRP3炎性体活化  

Liver X receptor agonists dampen NLRP3 inflammasome activation

作　　者：胡啸竹 李宁[1] 杜崇涛[1] 崔治华[2] 韩文瑜[1] 杨勇军[1] 陈巍[1] 

机构地区：[1]吉林大学动物医学学院,吉林长春130062 [2]吉林大学第一医院,吉林长春130021

出　　处：《中国兽医学报》2014年第2期259-263,共5页Chinese Journal of Veterinary Science

基　　金：国家自然科学基金资助项目(31172298);教育部新世纪优秀人才支持计划资助项目(NCET-09-0432)

摘　　要：为探讨肝X受体激动剂对NLRP3配体ATP诱导小鼠巨噬细胞炎性复合体活化的影响,应用荧光定量PCR方法测定肝X受体激动剂对LPS诱导的Pro-IL-1β、NLRP3等基因表达的影响,并用免疫蛋白印迹的方法检测Caspase-1的活化片段。结果证明,肝X受体(LXRs)激动剂能抑制NLRP3炎性体的活化。LXRs激动剂T0901317和GW3965显著抑制LPS联合ATP诱导的Caspase-1剪切成熟和IL-1β分泌,并且LXRs激动剂对NLRP3炎性体的抑制作用,部分源于其抑制NLRP3和IL-1β的基因转录。To investigate the effect of the liver X receptor agonist on the activation of inflammasome which was induced by NLRP3 agonist ATP in murine macrophage,the effect of LXRs agonists on Pro-IL-1/3,NLRP3 mRNA which was actived by LPS were tested by real-time PCR,the activity of Caspase-1 was detected by Western blot. In this study,we identify LXRs agonists as regulators of NLRP3 inflammasome activity. LXRs agonists potently blocked LPS＋ATP induced Caspase-1 ac tivation and IL-1β production. The inhibition may be partially related to transcriptional regulation, because T0901317 suppressed NLRP3 and IL-1β transcription in macrophage.

关 键 词：肝X受体激动剂 小鼠巨噬细胞 NLRP3炎性体 

分 类 号：S852.4[农业科学—基础兽医学]