摘要
目的探讨炎症体(inflammasome)在肝细胞内的表达,明确肝细胞内炎症体是否具有正常的炎症应答功能。方法以肝细胞株L02、HepG2为研究模型,RT-PCR、Real-time PCR检测LPS刺激及未刺激组caspase-1、IL-1β的mRNA的表达水平;Western blot检测NLRP3的表达和各刺激组胞内caspase-1活化;ELISA检测各刺激组上清中IL-1β和IL-18的分泌。结果 L02、HepG2细胞均表达NLRP3炎症体,LPS刺激促进肝细胞内caspase-1、IL-1β表达上调;内源性危险信号ATP能有效活化肝细胞内caspase-1酶原,促进IL-1β和IL-18分泌增加,caspase-1特异性抑制剂能特异性的抑制IL-1β、IL-18的分泌。结论肝实质细胞的NLRP3炎症体对内源性危险信号具有炎症应答功能,在肝内无菌性炎症的启动和维持中可能具有重要促进作用。
This study performed to investigate expression and function of NLRP3 inflammasome in hepatocytes. The expression of NLRP3 inflammasome in L02 and HepG2 cell lines was assayed by RT-PCR, Real- time PCR and Western blot; the activation of inflammasome was assay by Western blot and ELISA. Result showed that NLRP3 inflammasome was expressed in hepatocytes L02 and HepG2, and LPS inflammatory stimulation could upregulate the expression of NLRP3 inflammasome. Furthermore, the endogenous danger signal ATP also could promote hepatocytes to secrete IL-1β and IL-18 in a caspase-1 dependent manner. In conclusion, NLRP3 inflammasome in hepatocytes could initiate an inflammatory response to endogenous danger signals effectively, which implies a potential role of NLRP3 inflammasome in the pathogenesis of sterile inflammation.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2014年第2期129-132,共4页
Immunological Journal
基金
国家自然科学基金(31070796)
重庆市自然科学基金(CSTC2011BB5029,CSTC2011AB5034)
