Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet‐induced adipose tissue inflammation
Isoliquiritigenin, a component of Glycyrrhiza uralensis, is a potent inhibitor of the NLRP3 inflammasome, and suppresses diet‐induced obesity, adipose tissue inflammation, and metabolic disorders. Inflammasome activation initiates the development of many inflammatory diseases, including obesity and...
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| Veröffentlicht in: | Journal of leukocyte biology 2014-12, Vol.96 (6), p.1087-1100 |
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| creator | Honda, Hiroe Nagai, Yoshinori Matsunaga, Takayuki Okamoto, Naoki Watanabe, Yasuharu Tsuneyama, Koichi Hayashi, Hiroaki Fujii, Isao Ikutani, Masashi Hirai, Yoshikatsu Muraguchi, Atsushi Takatsu, Kiyoshi |
| description | Isoliquiritigenin, a component of Glycyrrhiza uralensis, is a potent inhibitor of the NLRP3 inflammasome, and suppresses diet‐induced obesity, adipose tissue inflammation, and metabolic disorders.
Inflammasome activation initiates the development of many inflammatory diseases, including obesity and type 2 diabetes. Therefore, agents that target discrete activation steps could represent very important drugs. We reported previously that ILG, a chalcone from Glycyrrhiza uralensis, inhibits LPS‐induced NF‐κB activation. Here, we show that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4. The inhibitory effect of ILG was stronger than that of parthenolide, a known inhibitor of the NLRP3 inflammasome. GL, a triterpenoid from G. uralensis, had similar inhibitory effects on NLRP3 activity, but high concentrations of GL were required. In contrast, activation of the AIM2 inflammasome was inhibited by GL but not by ILG. Moreover, GL inhibited NLRP3‐ and AIM2‐activated ASC oligomerization, whereas ILG inhibited NLRP3‐activated ASC oligomerization. Low concentrations of ILG were highly effective in IAPP‐induced IL‐1β production compared with the sulfonylurea drug glyburide. In vivo analyses revealed that ILG potently attenuated HFD‐induced obesity, hypercholesterolemia, and insulin resistance. Furthermore, ILG treatment improved HFD‐induced macrovesicular steatosis in the liver. Finally, ILG markedly inhibited diet‐induced adipose tissue inflammation and IL‐1β and caspase‐1 production in white adipose tissue in ex vivo culture. These results suggest that ILG is a potential drug target for treatment of NLRP3 inflammasome‐associated inflammatory diseases. |
| doi_str_mv | 10.1189/jlb.3A0114-005RR |
| format | Article |
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Inflammasome activation initiates the development of many inflammatory diseases, including obesity and type 2 diabetes. Therefore, agents that target discrete activation steps could represent very important drugs. We reported previously that ILG, a chalcone from Glycyrrhiza uralensis, inhibits LPS‐induced NF‐κB activation. Here, we show that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4. The inhibitory effect of ILG was stronger than that of parthenolide, a known inhibitor of the NLRP3 inflammasome. GL, a triterpenoid from G. uralensis, had similar inhibitory effects on NLRP3 activity, but high concentrations of GL were required. In contrast, activation of the AIM2 inflammasome was inhibited by GL but not by ILG. Moreover, GL inhibited NLRP3‐ and AIM2‐activated ASC oligomerization, whereas ILG inhibited NLRP3‐activated ASC oligomerization. Low concentrations of ILG were highly effective in IAPP‐induced IL‐1β production compared with the sulfonylurea drug glyburide. In vivo analyses revealed that ILG potently attenuated HFD‐induced obesity, hypercholesterolemia, and insulin resistance. Furthermore, ILG treatment improved HFD‐induced macrovesicular steatosis in the liver. Finally, ILG markedly inhibited diet‐induced adipose tissue inflammation and IL‐1β and caspase‐1 production in white adipose tissue in ex vivo culture. These results suggest that ILG is a potential drug target for treatment of NLRP3 inflammasome‐associated inflammatory diseases.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.3A0114-005RR</identifier><identifier>PMID: 25210146</identifier><language>eng</language><publisher>United States</publisher><subject><![CDATA[Adipose Tissue, White - drug effects ; Adipose Tissue, White - pathology ; AIM2 ; Animals ; Anti-Inflammatory Agents - isolation & purification ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Carrier Proteins - antagonists & inhibitors ; caspase‐1 ; Cell Line, Tumor ; Chalcones - isolation & purification ; Chalcones - pharmacology ; Chalcones - therapeutic use ; diabetes ; Diet, High-Fat - adverse effects ; DNA-Binding Proteins - metabolism ; Glyburide - pharmacology ; Glyburide - therapeutic use ; Glycyrrhiza ; Glycyrrhiza uralensis - chemistry ; Glycyrrhizic Acid - pharmacology ; Glycyrrhizic Acid - therapeutic use ; glycyrrhizin ; Humans ; Hypercholesterolemia - drug therapy ; IL‐1β ; Inflammasomes - drug effects ; Inflammation - prevention & control ; Insulin Resistance ; Interleukin-1beta - biosynthesis ; Islet Amyloid Polypeptide - antagonists & inhibitors ; Islet Amyloid Polypeptide - pharmacology ; Lipopolysaccharides - pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein ; obesity ; Obesity - drug therapy ; Obesity - prevention & control ; Specific Pathogen-Free Organisms]]></subject><ispartof>Journal of leukocyte biology, 2014-12, Vol.96 (6), p.1087-1100</ispartof><rights>2014 Society for Leukocyte Biology</rights><rights>2014 Society for Leukocyte Biology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4917-643b08f0d350d05eb1e4e8ba07c8b3c4068241e6150d1f1d996a93a525507e9b3</citedby><cites>FETCH-LOGICAL-c4917-643b08f0d350d05eb1e4e8ba07c8b3c4068241e6150d1f1d996a93a525507e9b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.3A0114-005RR$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.3A0114-005RR$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25210146$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Honda, Hiroe</creatorcontrib><creatorcontrib>Nagai, Yoshinori</creatorcontrib><creatorcontrib>Matsunaga, Takayuki</creatorcontrib><creatorcontrib>Okamoto, Naoki</creatorcontrib><creatorcontrib>Watanabe, Yasuharu</creatorcontrib><creatorcontrib>Tsuneyama, Koichi</creatorcontrib><creatorcontrib>Hayashi, Hiroaki</creatorcontrib><creatorcontrib>Fujii, Isao</creatorcontrib><creatorcontrib>Ikutani, Masashi</creatorcontrib><creatorcontrib>Hirai, Yoshikatsu</creatorcontrib><creatorcontrib>Muraguchi, Atsushi</creatorcontrib><creatorcontrib>Takatsu, Kiyoshi</creatorcontrib><title>Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet‐induced adipose tissue inflammation</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>Isoliquiritigenin, a component of Glycyrrhiza uralensis, is a potent inhibitor of the NLRP3 inflammasome, and suppresses diet‐induced obesity, adipose tissue inflammation, and metabolic disorders.
Inflammasome activation initiates the development of many inflammatory diseases, including obesity and type 2 diabetes. Therefore, agents that target discrete activation steps could represent very important drugs. We reported previously that ILG, a chalcone from Glycyrrhiza uralensis, inhibits LPS‐induced NF‐κB activation. Here, we show that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4. The inhibitory effect of ILG was stronger than that of parthenolide, a known inhibitor of the NLRP3 inflammasome. GL, a triterpenoid from G. uralensis, had similar inhibitory effects on NLRP3 activity, but high concentrations of GL were required. In contrast, activation of the AIM2 inflammasome was inhibited by GL but not by ILG. Moreover, GL inhibited NLRP3‐ and AIM2‐activated ASC oligomerization, whereas ILG inhibited NLRP3‐activated ASC oligomerization. Low concentrations of ILG were highly effective in IAPP‐induced IL‐1β production compared with the sulfonylurea drug glyburide. In vivo analyses revealed that ILG potently attenuated HFD‐induced obesity, hypercholesterolemia, and insulin resistance. Furthermore, ILG treatment improved HFD‐induced macrovesicular steatosis in the liver. Finally, ILG markedly inhibited diet‐induced adipose tissue inflammation and IL‐1β and caspase‐1 production in white adipose tissue in ex vivo culture. These results suggest that ILG is a potential drug target for treatment of NLRP3 inflammasome‐associated inflammatory diseases.</description><subject>Adipose Tissue, White - drug effects</subject><subject>Adipose Tissue, White - pathology</subject><subject>AIM2</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - isolation & purification</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Carrier Proteins - antagonists & inhibitors</subject><subject>caspase‐1</subject><subject>Cell Line, Tumor</subject><subject>Chalcones - isolation & purification</subject><subject>Chalcones - pharmacology</subject><subject>Chalcones - therapeutic use</subject><subject>diabetes</subject><subject>Diet, High-Fat - adverse effects</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Glyburide - pharmacology</subject><subject>Glyburide - therapeutic use</subject><subject>Glycyrrhiza</subject><subject>Glycyrrhiza uralensis - chemistry</subject><subject>Glycyrrhizic Acid - pharmacology</subject><subject>Glycyrrhizic Acid - therapeutic use</subject><subject>glycyrrhizin</subject><subject>Humans</subject><subject>Hypercholesterolemia - drug therapy</subject><subject>IL‐1β</subject><subject>Inflammasomes - drug effects</subject><subject>Inflammation - prevention & control</subject><subject>Insulin Resistance</subject><subject>Interleukin-1beta - biosynthesis</subject><subject>Islet Amyloid Polypeptide - antagonists & inhibitors</subject><subject>Islet Amyloid Polypeptide - pharmacology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>obesity</subject><subject>Obesity - drug therapy</subject><subject>Obesity - prevention & control</subject><subject>Specific Pathogen-Free Organisms</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1TAQhS0EopfCnhXykk3KOP6JvSxVgaIrQFewtpx4AlMl8W3sUHXHI_CMPAkpt3Tb1UhnvnM2H2MvBZwIYd2by6E9kacghKoA9G73iG2Ek7aSppGP2QYaJSqtAI7Ys5wvAUDWBp6yo1rXAoQyG3Z9kdNAVwvNVOg7TjRxyjzwfSo4FU7TD2qppJmnnn_a7r7INeqHMI4hpxF56Ar9DIXSxMMUeSQsf379pikuHUYeIu1TRl4o5wXvm7f4c_akD0PGF3f3mH17d_717EO1_fz-4ux0W3XKiaYySrZge4hSQwSNrUCFtg3QdLaVnQJjayXQiPUtehGdM8HJoGutoUHXymP2-rC7n9PVgrn4kXKHwxAmTEv2woI1spGgH0ZN7VxjFNgVhQPazSnnGXu_n2kM840X4G_N-NWMP5jx_8yslVd360s7Yrwv_FexAvoAXNOANw8O-o_btwJsI_8Cp4acLA</recordid><startdate>201412</startdate><enddate>201412</enddate><creator>Honda, Hiroe</creator><creator>Nagai, Yoshinori</creator><creator>Matsunaga, Takayuki</creator><creator>Okamoto, Naoki</creator><creator>Watanabe, Yasuharu</creator><creator>Tsuneyama, Koichi</creator><creator>Hayashi, Hiroaki</creator><creator>Fujii, Isao</creator><creator>Ikutani, Masashi</creator><creator>Hirai, Yoshikatsu</creator><creator>Muraguchi, Atsushi</creator><creator>Takatsu, Kiyoshi</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201412</creationdate><title>Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet‐induced adipose tissue inflammation</title><author>Honda, Hiroe ; Nagai, Yoshinori ; Matsunaga, Takayuki ; Okamoto, Naoki ; Watanabe, Yasuharu ; Tsuneyama, Koichi ; Hayashi, Hiroaki ; Fujii, Isao ; Ikutani, Masashi ; Hirai, Yoshikatsu ; Muraguchi, Atsushi ; Takatsu, Kiyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4917-643b08f0d350d05eb1e4e8ba07c8b3c4068241e6150d1f1d996a93a525507e9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adipose Tissue, White - drug effects</topic><topic>Adipose Tissue, White - pathology</topic><topic>AIM2</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - isolation & purification</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Carrier Proteins - antagonists & inhibitors</topic><topic>caspase‐1</topic><topic>Cell Line, Tumor</topic><topic>Chalcones - isolation & purification</topic><topic>Chalcones - pharmacology</topic><topic>Chalcones - therapeutic use</topic><topic>diabetes</topic><topic>Diet, High-Fat - adverse effects</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Glyburide - pharmacology</topic><topic>Glyburide - therapeutic use</topic><topic>Glycyrrhiza</topic><topic>Glycyrrhiza uralensis - chemistry</topic><topic>Glycyrrhizic Acid - pharmacology</topic><topic>Glycyrrhizic Acid - therapeutic use</topic><topic>glycyrrhizin</topic><topic>Humans</topic><topic>Hypercholesterolemia - drug therapy</topic><topic>IL‐1β</topic><topic>Inflammasomes - drug effects</topic><topic>Inflammation - prevention & control</topic><topic>Insulin Resistance</topic><topic>Interleukin-1beta - biosynthesis</topic><topic>Islet Amyloid Polypeptide - antagonists & inhibitors</topic><topic>Islet Amyloid Polypeptide - pharmacology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>obesity</topic><topic>Obesity - drug therapy</topic><topic>Obesity - prevention & control</topic><topic>Specific Pathogen-Free Organisms</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Honda, Hiroe</creatorcontrib><creatorcontrib>Nagai, Yoshinori</creatorcontrib><creatorcontrib>Matsunaga, Takayuki</creatorcontrib><creatorcontrib>Okamoto, Naoki</creatorcontrib><creatorcontrib>Watanabe, Yasuharu</creatorcontrib><creatorcontrib>Tsuneyama, Koichi</creatorcontrib><creatorcontrib>Hayashi, Hiroaki</creatorcontrib><creatorcontrib>Fujii, Isao</creatorcontrib><creatorcontrib>Ikutani, Masashi</creatorcontrib><creatorcontrib>Hirai, Yoshikatsu</creatorcontrib><creatorcontrib>Muraguchi, Atsushi</creatorcontrib><creatorcontrib>Takatsu, Kiyoshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Honda, Hiroe</au><au>Nagai, Yoshinori</au><au>Matsunaga, Takayuki</au><au>Okamoto, Naoki</au><au>Watanabe, Yasuharu</au><au>Tsuneyama, Koichi</au><au>Hayashi, Hiroaki</au><au>Fujii, Isao</au><au>Ikutani, Masashi</au><au>Hirai, Yoshikatsu</au><au>Muraguchi, Atsushi</au><au>Takatsu, Kiyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet‐induced adipose tissue inflammation</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2014-12</date><risdate>2014</risdate><volume>96</volume><issue>6</issue><spage>1087</spage><epage>1100</epage><pages>1087-1100</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>Isoliquiritigenin, a component of Glycyrrhiza uralensis, is a potent inhibitor of the NLRP3 inflammasome, and suppresses diet‐induced obesity, adipose tissue inflammation, and metabolic disorders.
Inflammasome activation initiates the development of many inflammatory diseases, including obesity and type 2 diabetes. Therefore, agents that target discrete activation steps could represent very important drugs. We reported previously that ILG, a chalcone from Glycyrrhiza uralensis, inhibits LPS‐induced NF‐κB activation. Here, we show that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4. The inhibitory effect of ILG was stronger than that of parthenolide, a known inhibitor of the NLRP3 inflammasome. GL, a triterpenoid from G. uralensis, had similar inhibitory effects on NLRP3 activity, but high concentrations of GL were required. In contrast, activation of the AIM2 inflammasome was inhibited by GL but not by ILG. Moreover, GL inhibited NLRP3‐ and AIM2‐activated ASC oligomerization, whereas ILG inhibited NLRP3‐activated ASC oligomerization. Low concentrations of ILG were highly effective in IAPP‐induced IL‐1β production compared with the sulfonylurea drug glyburide. In vivo analyses revealed that ILG potently attenuated HFD‐induced obesity, hypercholesterolemia, and insulin resistance. Furthermore, ILG treatment improved HFD‐induced macrovesicular steatosis in the liver. Finally, ILG markedly inhibited diet‐induced adipose tissue inflammation and IL‐1β and caspase‐1 production in white adipose tissue in ex vivo culture. These results suggest that ILG is a potential drug target for treatment of NLRP3 inflammasome‐associated inflammatory diseases.</abstract><cop>United States</cop><pmid>25210146</pmid><doi>10.1189/jlb.3A0114-005RR</doi><tpages>14</tpages></addata></record> |
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| ispartof | Journal of leukocyte biology, 2014-12, Vol.96 (6), p.1087-1100 |
| issn | 0741-5400 1938-3673 |
| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adipose Tissue, White - drug effects Adipose Tissue, White - pathology AIM2 Animals Anti-Inflammatory Agents - isolation & purification Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Carrier Proteins - antagonists & inhibitors caspase‐1 Cell Line, Tumor Chalcones - isolation & purification Chalcones - pharmacology Chalcones - therapeutic use diabetes Diet, High-Fat - adverse effects DNA-Binding Proteins - metabolism Glyburide - pharmacology Glyburide - therapeutic use Glycyrrhiza Glycyrrhiza uralensis - chemistry Glycyrrhizic Acid - pharmacology Glycyrrhizic Acid - therapeutic use glycyrrhizin Humans Hypercholesterolemia - drug therapy IL‐1β Inflammasomes - drug effects Inflammation - prevention & control Insulin Resistance Interleukin-1beta - biosynthesis Islet Amyloid Polypeptide - antagonists & inhibitors Islet Amyloid Polypeptide - pharmacology Lipopolysaccharides - pharmacology Male Mice Mice, Inbred C57BL NLR Family, Pyrin Domain-Containing 3 Protein obesity Obesity - drug therapy Obesity - prevention & control Specific Pathogen-Free Organisms |
| title | Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet‐induced adipose tissue inflammation |
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