Peroxisome proliferator-activated receptor-delta agonist ameliorated inflammasome activation in nonalcoholic fatty liver disease

To evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver disease (NAFLD) models. Male C57BL/6J mice were classified according to control or high fat diet (HFD) with or without PPAR-δ agonist (GW) over...

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Vydáno v:	World journal of gastroenterology : WJG Ročník 21; číslo 45; s. 12787 - 12799
Hlavní autoři:	Lee, Hyun Jung, Yeon, Jong Eun, Ko, Eun Jung, Yoon, Eileen L, Suh, Sang Jun, Kang, Keunhee, Kim, Hae Rim, Kang, Seoung Hee, Yoo, Yang Jae, Je, Jihye, Lee, Beom Jae, Kim, Ji Hoon, Seo, Yeon Seok, Yim, Hyung Joon, Byun, Kwan Soo
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 07.12.2015
Témata:	Animals Anti-Inflammatory Agents - pharmacology Blood Glucose - drug effects Blood Glucose - metabolism Cytoprotection Diet, High-Fat Disease Models, Animal Gene Expression Regulation Hep G2 Cells Hepatocytes - drug effects Hepatocytes - metabolism Hepatocytes - pathology Humans Inflammasomes - antagonists & inhibitors Inflammasomes - genetics Inflammasomes - metabolism Inflammation Mediators - metabolism Lipopolysaccharides Liver - drug effects Liver - metabolism Liver - pathology Male Mice, Inbred C57BL Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Non-alcoholic Fatty Liver Disease - prevention & control Oxidative Stress - drug effects Palmitic Acid - toxicity PPAR delta - agonists PPAR delta - metabolism Signal Transduction - drug effects Thiazoles - pharmacology Time Factors Nucleotide-binding and oligomerization domain-like receptor Inflammasome Nonalcoholic fatty liver disease Nonalcoholic steatohepatitis Peroxisome proliferator-activated receptors delta
ISSN:	2219-2840
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Popis
Shrnutí:	To evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver disease (NAFLD) models. Male C57BL/6J mice were classified according to control or high fat diet (HFD) with or without PPAR-δ agonist (GW) over period of 12 wk [control, HFD, HFD + lipopolysaccharide (LPS), HFD + LPS + GW group]. HepG2 cells were exposed to palmitic acid (PA) and/or LPS in the absence or presence of GW. HFD caused glucose intolerance and hepatic steatosis. In mice fed an HFD with LPS, caspase-1 and interleukin (IL)-1β in the liver were significantly increased. Treatment with GW ameliorated the steatosis and inhibited overexpression of pro-inflammatory cytokines. In HepG2 cells, PA and LPS treatment markedly increased mRNA of several nucleotide-binding and oligomerization domain-like receptor family members (NLRP3, NLRP6, and NLRP10), caspase-1 and IL-1β. PA and LPS also exaggerated reactive oxygen species production. All of the above effects of PA and LPS were reduced by GW. GW also enhanced the phosphorylation of AMPK-α. PPAR-δ agonist reduces fatty acid-induced inflammation and steatosis by suppressing inflammasome activation. Targeting the inflammasome by the PPAR-δ agonist may have therapeutic implication for NAFLD.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	2219-2840
DOI:	10.3748/wjg.v21.i45.12787