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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| Vydané v: | World journal of gastroenterology : WJG Ročník 21; číslo 45; s. 12787 - 12799 |
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| Hlavní autori: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
07.12.2015
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| ISSN: | 2219-2840 |
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| Abstract | 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. |
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| AbstractList | 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. AIMTo evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver disease (NAFLD) models.METHODSMale 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.RESULTSHFD 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.CONCLUSIONPPAR-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. |
| Author | Kang, Seoung Hee Kim, Ji Hoon Seo, Yeon Seok Lee, Hyun Jung Suh, Sang Jun Kang, Keunhee Lee, Beom Jae Yim, Hyung Joon Byun, Kwan Soo Kim, Hae Rim Yoon, Eileen L Je, Jihye Ko, Eun Jung Yeon, Jong Eun Yoo, Yang Jae |
| Author_xml | – sequence: 1 givenname: Hyun Jung surname: Lee fullname: Lee, Hyun Jung organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 2 givenname: Jong Eun surname: Yeon fullname: Yeon, Jong Eun organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 3 givenname: Eun Jung surname: Ko fullname: Ko, Eun Jung organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 4 givenname: Eileen L surname: Yoon fullname: Yoon, Eileen L organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 5 givenname: Sang Jun surname: Suh fullname: Suh, Sang Jun organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 6 givenname: Keunhee surname: Kang fullname: Kang, Keunhee organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 7 givenname: Hae Rim surname: Kim fullname: Kim, Hae Rim organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 8 givenname: Seoung Hee surname: Kang fullname: Kang, Seoung Hee organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 9 givenname: Yang Jae surname: Yoo fullname: Yoo, Yang Jae organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 10 givenname: Jihye surname: Je fullname: Je, Jihye organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 11 givenname: Beom Jae surname: Lee fullname: Lee, Beom Jae organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 12 givenname: Ji Hoon surname: Kim fullname: Kim, Ji Hoon organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 13 givenname: Yeon Seok surname: Seo fullname: Seo, Yeon Seok organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 14 givenname: Hyung Joon surname: Yim fullname: Yim, Hyung Joon organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea – sequence: 15 givenname: Kwan Soo surname: Byun fullname: Byun, Kwan Soo organization: Hyun Jung Lee, Jong Eun Yeon, Eun Jung Ko, Eileen L Yoon, Sang Jun Suh, Keunhee Kang, Hae Rim Kim, Seoung Hee Kang, Yang Jae Yoo, Jihye Je, Beom Jae Lee, Ji Hoon Kim, Yeon Seok Seo, Hyung Joon Yim, Kwan Soo Byun, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-703, South Korea |
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| Keywords | Nucleotide-binding and oligomerization domain-like receptor Inflammasome Nonalcoholic fatty liver disease Nonalcoholic steatohepatitis Peroxisome proliferator-activated receptors delta |
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| Snippet | To evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver... AIMTo evaluate the inflammasome activation and the effect of peroxisome proliferator-activated receptors (PPAR)-δ agonist treatment in nonalcoholic fatty liver... |
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| SubjectTerms | 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 |
| Title | Peroxisome proliferator-activated receptor-delta agonist ameliorated inflammasome activation in nonalcoholic fatty liver disease |
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