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Cited 49 time in webofscience Cited 51 time in scopus
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Peroxisome proliferator-activated receptor-delta agonist ameliorated inflammasome activation in nonalcoholic fatty liver disease

Authors
Lee, Hyun JungYeon, Jong EunKo, Eun JungYoon, Eileen L.Suh, Sang JunKang, KeunheeKim, Hae RimKang, Seoung HeeYoo, Yang JaeJe, JihyeLee, Beom JaeKim, Ji HoonSeo, Yeon SeokYim, Hyung JoonByun, Kwan Soo
Issue Date
Dec-2015
Publisher
Baishideng Publishing Group
Keywords
Nonalcoholic fatty liver disease; Nonalcoholic steatohepatitis; Inflammasome; Nucleotide-binding and oligomerization domain-like receptor; Peroxisome proliferator-activated receptors delta
Citation
World Journal of Gastroenterology, v.21, no.45, pp 12787 - 12799
Pages
13
Indexed
SCIE
SCOPUS
Journal Title
World Journal of Gastroenterology
Volume
21
Number
45
Start Page
12787
End Page
12799
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/7226
DOI
10.3748/wjg.v21.i45.12787
ISSN
1007-9327
2219-2840
Abstract
AIM: To evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver disease (NAFLD) models. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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Seo, Yeon Seok
Anam Hospital (Department of Gastroenterology and Hepatology, Anam Hospital)
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