RISS 검색 - 국내학술지논문

무료
기관 내 무료
유료

내보내기
내책장담기
한글로보기

정확도순

내림차순

내림차순

10개씩 출력

1
Inflammation‐associated interleukin‐6/signal transducer and activator of transcription 3 activation ameliorates alcoholic and nonalcoholic fatty liver diseases in interleukin‐10–deficient mice

Miller, Andrew M.,Wang, Hua,Bertola, Adeline,Park, Ogyi,Horiguchi, Norio,Hwan Ki, Sung,Yin, Shi,Lafdil, Fouad,Gao, Bin Wiley Subscription Services, Inc., A Wiley Company 2011 Hepatology Vol.54 No.3
- 원문보기
AbstractAlcoholic and nonalcoholic steatohepatitis are characterized by fatty liver plus inflammation. It is generally believed that steatosis promotes inflammation, whereas inflammation in turn aggregates steatosis. Thus, we hypothesized the deletion of interleukin (IL)‐10, a key anti‐inflammatory cytokine, exacerbates liver inflammation, steatosis, and hepatocellular damage in alcoholic and nonalcoholic fatty liver disease models that were achieved via feeding mice with a liquid diet containing 5% ethanol for 4 weeks or a high‐fat diet (HFD) for 12 weeks, respectively. IL‐10 knockout (IL‐10−/−) mice and several other strains of genetically modified mice were generated and used. Compared with wild‐type mice, IL‐10−/− mice had greater liver inflammatory response with higher levels of IL‐6 and hepatic signal transducer and activator of transcription 3 (STAT3) activation, but less steatosis and hepatocellular damage after alcohol or HFD feeding. An additional deletion of IL‐6 or hepatic STAT3 restored steatosis and hepatocellular damage but further enhanced liver inflammatory response in IL‐10−/− mice. In addition, the hepatic expression of sterol regulatory element‐binding protein 1 and key downstream lipogenic proteins and enzymes in fatty acid synthesis were down‐regulated in IL‐10−/− mice. Conversely, IL‐10−/− mice displayed enhanced levels of phosphorylated adenosine monophosphate‐activated protein kinase and its downstream targets including phosphorylated acetyl‐coenzyme A carboxylase and carnitine palmitoyltransferase 1 in the liver. Such dysregulations were corrected in IL‐10−/−IL‐6−/− or IL‐10−/−STAT3Hep−/− double knockout mice. Conclusion: IL‐10−/− mice are prone to liver inflammatory response but are resistant to steatosis and hepatocellular damage induced by ethanol or HFD feeding. Resistance to steatosis in these mice is attributable to elevation of inflammation‐associated hepatic IL‐6/STAT3 activation that subsequently down‐regulates lipogenic genes but up‐regulates fatty acid oxidation‐associated genes in the liver. (HEPATOLOGY 2011; 54:846–856)

내보내기
내책장담기
한글로보기

정확도순

내림차순

내림차순

10개씩 출력

맨처음 페이지로 1 맨끝 페이지로

상세검색

RISS 보유자료

상세검색

해외전자자료

연관 검색어 추천