- 영문명
- Effects of NLRP3 inflammasome knockdown on sirtuin pathway and inflammatory markers in AML12 mouse hepatocytes
- 발행기관
- 전남대학교 생활과학연구소
- 저자명
- 이희재(Hee Jae Lee) 임소영(So Young Lim) 양수진(Soo Jin Yang)
- 간행물 정보
- 『生活科學硏究』生活科學硏究 第23輯, 33~41쪽, 전체 9쪽
- 주제분류
- 자연과학 > 생활/식품과학
- 파일형태
- 발행일자
- 2013.12.30

국문 초록
영문 초록
Nucleotide binding and oligomerization domain (NOD)-like receptor family, pryin domain containing 3 (NLRP3) inflammasome is the protein complex regulating interleukin-1 (IL-1) secretion and consists of NLRP3, apoptosis-associated speck-like protein containing a caspase activation recruitment domain (ASC), and caspase 1. Initial studies on inflammasomes were primarily focused on innate immunity; however, recent reports have demonstrated that NLRP3 inflammasome may be responsible for the development and progression of inflammation-related diseases including obesity and type 2 diabetes. The aim of this study was to investigate the effects of NLRP3 knockdown on the sirtuin pathway and inflammation in AML12 mouse hepatocytes. RNA interference (RNAi)-mediated gene silencing was performed for NLRP3 knockdown. After 48 h of transfection with small interfering RNA(siRNA) targeting NLRP3, components of sirtuin pathway and markers of inflammation were analysed in cell lysates. NLRP3 knockdown for 48 h had no effect on hepatocyte morphology and cell number. The transfection efficiency and knockdown rate of NLRP3 were confirmed. NLRP3 knockdown in hepatocytes had no effect on sirtuin pathway-related
factors: sirtuin 1 (Sirt1), Sirt6, adiponectin, and peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-1 alpha). However, the NLRP3 knockdown in hepatocytes down-regulated those of pro-inflammatory markers such as IL-6 and tumor necrosis factor-alpha (TNF-alpha). Our results demonstrate that RNAi-mediated inhibition of NLRP3 inflammasome alters inflammation in hepatocytes without affecting sirtuin pathway. We propose NLRP3 as a potential therapeutic target for inflammationrelated diseases.
목차
Ⅰ. 서론
Ⅱ. 재료 및 방법
Ⅲ. 결과 및 고찰
Ⅳ. 요약 및 결론
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