Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-κB/ NLRP3/GSDMD signals in human gingival fibroblasts
•LPS/ATP induced pyroptosis through activating NF-κB/NLRP3/GSDMD signals in HGFs.•Interdomain cleavage of GSDMD by caspase-1 played an important role in pyroptosis.•High levels of interleukin-1β can cause an HGF inflammatory response.•Isoliquiritigenin attenuated LPS/ATP-induced pyroptosis and the r...
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| Veröffentlicht in: | International immunopharmacology 2021-12, Vol.101 (Pt B), p.108338-108338, Article 108338 |
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| creator | Lv, Xiaofang Fan, Chun Jiang, Zhongxin Wang, Wenxuan Qiu, Xu Ji, Qiuxia |
| description | •LPS/ATP induced pyroptosis through activating NF-κB/NLRP3/GSDMD signals in HGFs.•Interdomain cleavage of GSDMD by caspase-1 played an important role in pyroptosis.•High levels of interleukin-1β can cause an HGF inflammatory response.•Isoliquiritigenin attenuated LPS/ATP-induced pyroptosis and the release of IL-1β.
To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-κB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-κB/NLRP3/GSDMD signals.
Periodontitis was optimally simulated using a combination of P. gingivalis-LPS and ATP. The expression levels of genes and proteins of NF-κB, NLRP3 inflammasome, GSDMD, and IL-1β was characterized by qRT-PCR, western blotting and ELISA. The 2ʹ,7ʹ‑dichlorodihydrofluorescein diacetate fluorescence probe was used to determine the intracellular ROS level. Hoechst 33342 and PI double staining, cytotoxicity assay, and caspase-1 activity assay were used to confirm the influence of ISL on pyroptosis in P. gingivalis-LPS/ATP-treated HGFs.
P. gingivalis-LPS/ATP stimulation significantly promoted expression of NF-κB, the NLRP3 inflammasome, GSDMD, and IL-1β at gene and protein levels. The proportion of membrane-damaged cells, caspase-1 activity, and the release of lactate dehydrogenase (LDH) were also elevated. However, pretreatment with ISL observably suppressed these effects.
P. gingivalis-LPS/ATP induced pyroptosis in HGFs by activating NF-κB/NLRP3/GSDMD signals and ISL attenuated P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting these signals. This evidence may provide a new direction for the treatment of periodontitis. |
| doi_str_mv | 10.1016/j.intimp.2021.108338 |
| format | Article |
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To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-κB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-κB/NLRP3/GSDMD signals.
Periodontitis was optimally simulated using a combination of P. gingivalis-LPS and ATP. The expression levels of genes and proteins of NF-κB, NLRP3 inflammasome, GSDMD, and IL-1β was characterized by qRT-PCR, western blotting and ELISA. The 2ʹ,7ʹ‑dichlorodihydrofluorescein diacetate fluorescence probe was used to determine the intracellular ROS level. Hoechst 33342 and PI double staining, cytotoxicity assay, and caspase-1 activity assay were used to confirm the influence of ISL on pyroptosis in P. gingivalis-LPS/ATP-treated HGFs.
P. gingivalis-LPS/ATP stimulation significantly promoted expression of NF-κB, the NLRP3 inflammasome, GSDMD, and IL-1β at gene and protein levels. The proportion of membrane-damaged cells, caspase-1 activity, and the release of lactate dehydrogenase (LDH) were also elevated. However, pretreatment with ISL observably suppressed these effects.
P. gingivalis-LPS/ATP induced pyroptosis in HGFs by activating NF-κB/NLRP3/GSDMD signals and ISL attenuated P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting these signals. This evidence may provide a new direction for the treatment of periodontitis.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2021.108338</identifier><identifier>PMID: 34794890</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adenosine triphosphate ; Adenosine Triphosphate - pharmacology ; ATP ; Caspase-1 ; Cells, Cultured ; Chalcones ; Cytotoxicity ; Enzyme-linked immunosorbent assay ; Fibroblasts ; Fibroblasts - drug effects ; Fluorescence ; Fluorescent indicators ; Gene expression ; Gingiva - metabolism ; GSDMD ; Humans ; I-kappa B Proteins - metabolism ; IL-1β ; Inflammasomes ; Inflammasomes - metabolism ; Interleukin-1beta ; Intracellular Signaling Peptides and Proteins - metabolism ; Isoliquiritigenin ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Lactic acid ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; NF-kappa B - metabolism ; NF-κB ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Periodontitis ; Phosphate-Binding Proteins - metabolism ; Pore Forming Cytotoxic Proteins ; Porphyromonas gingivalis ; Proteins ; Pyroptosis ; Pyroptosis - drug effects ; Signal Transduction - drug effects ; Toxicity ; Western blotting</subject><ispartof>International immunopharmacology, 2021-12, Vol.101 (Pt B), p.108338-108338, Article 108338</ispartof><rights>2021 Elsevier B.V.</rights><rights>Copyright © 2021 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Dec 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-38d5362dface4761fd0bd60e853c51747526b33686ce69a090c19d5935e9ba483</citedby><cites>FETCH-LOGICAL-c390t-38d5362dface4761fd0bd60e853c51747526b33686ce69a090c19d5935e9ba483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2021.108338$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34794890$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lv, Xiaofang</creatorcontrib><creatorcontrib>Fan, Chun</creatorcontrib><creatorcontrib>Jiang, Zhongxin</creatorcontrib><creatorcontrib>Wang, Wenxuan</creatorcontrib><creatorcontrib>Qiu, Xu</creatorcontrib><creatorcontrib>Ji, Qiuxia</creatorcontrib><title>Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-κB/ NLRP3/GSDMD signals in human gingival fibroblasts</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>•LPS/ATP induced pyroptosis through activating NF-κB/NLRP3/GSDMD signals in HGFs.•Interdomain cleavage of GSDMD by caspase-1 played an important role in pyroptosis.•High levels of interleukin-1β can cause an HGF inflammatory response.•Isoliquiritigenin attenuated LPS/ATP-induced pyroptosis and the release of IL-1β.
To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-κB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-κB/NLRP3/GSDMD signals.
Periodontitis was optimally simulated using a combination of P. gingivalis-LPS and ATP. The expression levels of genes and proteins of NF-κB, NLRP3 inflammasome, GSDMD, and IL-1β was characterized by qRT-PCR, western blotting and ELISA. The 2ʹ,7ʹ‑dichlorodihydrofluorescein diacetate fluorescence probe was used to determine the intracellular ROS level. Hoechst 33342 and PI double staining, cytotoxicity assay, and caspase-1 activity assay were used to confirm the influence of ISL on pyroptosis in P. gingivalis-LPS/ATP-treated HGFs.
P. gingivalis-LPS/ATP stimulation significantly promoted expression of NF-κB, the NLRP3 inflammasome, GSDMD, and IL-1β at gene and protein levels. The proportion of membrane-damaged cells, caspase-1 activity, and the release of lactate dehydrogenase (LDH) were also elevated. However, pretreatment with ISL observably suppressed these effects.
P. gingivalis-LPS/ATP induced pyroptosis in HGFs by activating NF-κB/NLRP3/GSDMD signals and ISL attenuated P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting these signals. This evidence may provide a new direction for the treatment of periodontitis.</description><subject>Adenosine triphosphate</subject><subject>Adenosine Triphosphate - pharmacology</subject><subject>ATP</subject><subject>Caspase-1</subject><subject>Cells, Cultured</subject><subject>Chalcones</subject><subject>Cytotoxicity</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fluorescence</subject><subject>Fluorescent indicators</subject><subject>Gene expression</subject><subject>Gingiva - metabolism</subject><subject>GSDMD</subject><subject>Humans</subject><subject>I-kappa B Proteins - metabolism</subject><subject>IL-1β</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Interleukin-1beta</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Isoliquiritigenin</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Periodontitis</subject><subject>Phosphate-Binding Proteins - metabolism</subject><subject>Pore Forming Cytotoxic Proteins</subject><subject>Porphyromonas gingivalis</subject><subject>Proteins</subject><subject>Pyroptosis</subject><subject>Pyroptosis - drug effects</subject><subject>Signal Transduction - drug effects</subject><subject>Toxicity</subject><subject>Western blotting</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhyMEoqXwBghZ4sIlu3b8J_YFqbS0VFrKipaz5ThOOqusk9rJSvsQfaE-BM-EVyk9cOA01uib38jzZdl7ghcEE7HcLMCPsB0WBS5IaklK5YvsmMhS5qTE_GV6c1HmvBTqKHsT4wbj1GfkdXZEWamYVPg4e7iKfQf3EwQYoXUePDJd53ZgRhfReoFa8C3sTAcxX61vlqe36xx8PVlXo2Ef-mHsI0RU7RH4O6hSiG_R9UX--_HLEl2vfq7p8vLm_Ps5itB608WEobtpa_xzMGqgCn3VmTjGt9mrJkHu3VM9yX5dfL09-5avflxenZ2ucksVHnMqa05FUTfGOlYK0tS4qgV2klPLSclKXoiKUiGFdUIZrLAlquaKcqcqwyQ9yT7NuUPo7ycXR72FaF3XGe_6KeqCK0UkwZQl9OM_6KafwuEruhAFU1IyWiSKzZQNfYzBNXoIsDVhrwnWB116o2dd-qBLz7rS2Ien8Knauvp56K-fBHyeAZeusQMXdLTgfLo-BGdHXffw_w1_AKEWqIs</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Lv, Xiaofang</creator><creator>Fan, Chun</creator><creator>Jiang, Zhongxin</creator><creator>Wang, Wenxuan</creator><creator>Qiu, Xu</creator><creator>Ji, Qiuxia</creator><general>Elsevier B.V</general><general>Elsevier BV</general><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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>202112</creationdate><title>Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-κB/ NLRP3/GSDMD signals in human gingival fibroblasts</title><author>Lv, Xiaofang ; Fan, Chun ; Jiang, Zhongxin ; Wang, Wenxuan ; Qiu, Xu ; Ji, Qiuxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-38d5362dface4761fd0bd60e853c51747526b33686ce69a090c19d5935e9ba483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenosine triphosphate</topic><topic>Adenosine Triphosphate - pharmacology</topic><topic>ATP</topic><topic>Caspase-1</topic><topic>Cells, Cultured</topic><topic>Chalcones</topic><topic>Cytotoxicity</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fluorescence</topic><topic>Fluorescent indicators</topic><topic>Gene expression</topic><topic>Gingiva - metabolism</topic><topic>GSDMD</topic><topic>Humans</topic><topic>I-kappa B Proteins - metabolism</topic><topic>IL-1β</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Interleukin-1beta</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Isoliquiritigenin</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Periodontitis</topic><topic>Phosphate-Binding Proteins - metabolism</topic><topic>Pore Forming Cytotoxic Proteins</topic><topic>Porphyromonas gingivalis</topic><topic>Proteins</topic><topic>Pyroptosis</topic><topic>Pyroptosis - drug effects</topic><topic>Signal Transduction - drug effects</topic><topic>Toxicity</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lv, Xiaofang</creatorcontrib><creatorcontrib>Fan, Chun</creatorcontrib><creatorcontrib>Jiang, Zhongxin</creatorcontrib><creatorcontrib>Wang, Wenxuan</creatorcontrib><creatorcontrib>Qiu, Xu</creatorcontrib><creatorcontrib>Ji, Qiuxia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lv, Xiaofang</au><au>Fan, Chun</au><au>Jiang, Zhongxin</au><au>Wang, Wenxuan</au><au>Qiu, Xu</au><au>Ji, Qiuxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-κB/ NLRP3/GSDMD signals in human gingival fibroblasts</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2021-12</date><risdate>2021</risdate><volume>101</volume><issue>Pt B</issue><spage>108338</spage><epage>108338</epage><pages>108338-108338</pages><artnum>108338</artnum><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>•LPS/ATP induced pyroptosis through activating NF-κB/NLRP3/GSDMD signals in HGFs.•Interdomain cleavage of GSDMD by caspase-1 played an important role in pyroptosis.•High levels of interleukin-1β can cause an HGF inflammatory response.•Isoliquiritigenin attenuated LPS/ATP-induced pyroptosis and the release of IL-1β.
To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-κB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-κB/NLRP3/GSDMD signals.
Periodontitis was optimally simulated using a combination of P. gingivalis-LPS and ATP. The expression levels of genes and proteins of NF-κB, NLRP3 inflammasome, GSDMD, and IL-1β was characterized by qRT-PCR, western blotting and ELISA. The 2ʹ,7ʹ‑dichlorodihydrofluorescein diacetate fluorescence probe was used to determine the intracellular ROS level. Hoechst 33342 and PI double staining, cytotoxicity assay, and caspase-1 activity assay were used to confirm the influence of ISL on pyroptosis in P. gingivalis-LPS/ATP-treated HGFs.
P. gingivalis-LPS/ATP stimulation significantly promoted expression of NF-κB, the NLRP3 inflammasome, GSDMD, and IL-1β at gene and protein levels. The proportion of membrane-damaged cells, caspase-1 activity, and the release of lactate dehydrogenase (LDH) were also elevated. However, pretreatment with ISL observably suppressed these effects.
P. gingivalis-LPS/ATP induced pyroptosis in HGFs by activating NF-κB/NLRP3/GSDMD signals and ISL attenuated P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting these signals. This evidence may provide a new direction for the treatment of periodontitis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>34794890</pmid><doi>10.1016/j.intimp.2021.108338</doi><tpages>1</tpages></addata></record> |
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| ispartof | International immunopharmacology, 2021-12, Vol.101 (Pt B), p.108338-108338, Article 108338 |
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| subjects | Adenosine triphosphate Adenosine Triphosphate - pharmacology ATP Caspase-1 Cells, Cultured Chalcones Cytotoxicity Enzyme-linked immunosorbent assay Fibroblasts Fibroblasts - drug effects Fluorescence Fluorescent indicators Gene expression Gingiva - metabolism GSDMD Humans I-kappa B Proteins - metabolism IL-1β Inflammasomes Inflammasomes - metabolism Interleukin-1beta Intracellular Signaling Peptides and Proteins - metabolism Isoliquiritigenin L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid Lipopolysaccharides Lipopolysaccharides - pharmacology NF-kappa B - metabolism NF-κB NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Periodontitis Phosphate-Binding Proteins - metabolism Pore Forming Cytotoxic Proteins Porphyromonas gingivalis Proteins Pyroptosis Pyroptosis - drug effects Signal Transduction - drug effects Toxicity Western blotting |
| title | Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-κB/ NLRP3/GSDMD signals in human gingival fibroblasts |
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