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학술저널

NLRP3 인플라마좀 유전자 발현 억제가 시르투인 경로와 염증조절인자에 미치는 영향

Effects of NLRP3 inflammasome knockdown on sirtuin pathway and inflammatory markers in AML12 mouse hepatocytes

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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.

Ⅰ. 서론

Ⅱ. 재료 및 방법

Ⅲ. 결과 및 고찰

Ⅳ. 요약 및 결론

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