Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation
Abstract Background NLRP3 inflammasome activation is recently reported to be linked to the pathogenesis of sepsis. Artemisinin is shown to play beneficial effects in sepsis. However, the impacts of artemisinin on burn sepsis have not been investigated. This study is designed to investigate the role...
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| Veröffentlicht in: | The American journal of emergency medicine 2016-05, Vol.34 (5), p.772-777 |
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| creator | Long, Huibao, MD Xu, Bincan, MM Luo, Yanling, MM Luo, Keqin, MM |
| description | Abstract Background NLRP3 inflammasome activation is recently reported to be linked to the pathogenesis of sepsis. Artemisinin is shown to play beneficial effects in sepsis. However, the impacts of artemisinin on burn sepsis have not been investigated. This study is designed to investigate the role of artemisinin in burn sepsis and the involvement of NLRP3 inflammasome activation. Methods Male BALB/c mice were randomly divided into sham burn, burn, burn sepsis, and artemisinin treated groups. Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Adhesion molecules and neutrophil infiltration in lung and heart were detected by real-time polymerase chain reaction. Mortality rates were monitored. Artemisinin was added to Raw 264.7 cells that were stimulated with burn sepsis serum in the presence/absence of an inhibitor of NLRP3 inflammasome, 3, 4-methylenedioxy- β -nitrostyrene. Interleukin (IL) 1 β and IL-18 messenger RNA expression as well as NLRP3 and caspase 1 protein were measured. Results Production of inflammatory cytokines in serum, levels of adhesion molecules and neutrophil infiltration in lung and heart, and mortality rate of burn septic mice were significantly higher than those of control. These effects were attenuated by artemisinin. Artemisinin down-regulated protein levels of NLRP3 and caspase 1 and inhibited the increases of IL-1 β and IL-18 messenger RNA expression from Raw 264.7 cells that were stimulated with burn sepsis serum. These effects of artemisinin were not further strengthened in the presence of 4-methylenedioxy- β -nitrostyrene. Conclusion Artemisinin protects mice from burn sepsis by attenuating the inflammatory response and alleviating inflammatory infiltration in vital organs, likely through inhibiting the activation of NLRP3 inflammasome. |
| doi_str_mv | 10.1016/j.ajem.2015.12.075 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1794495947</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0735675715011572</els_id><sourcerecordid>4038366881</sourcerecordid><originalsourceid>FETCH-LOGICAL-c472t-8936e042f2c628bc8940f34f63893960740d0eb1d2912bfdb9f5b2af9c2989ee3</originalsourceid><addsrcrecordid>eNqNkl2L1DAUhoMo7rj6B7yQgjfetCYnSdOACMviFwwqftwa0vR0JmM_ZpN0Yf-9KbMq7IV4VUif98B7nkPIU0YrRln98lDZA44VUCYrBhVV8h7ZMMmhbJhi98mGKi7LWkl1Rh7FeKCUMSHFQ3IGdcMpsHpDflyEhKOPfvJTcQxzQpdiMXqHhd1ZP8VUtEuYiojH6GOR9mFedvvCT3vf-uSnXfFx--Uzzw_9YMfRxnnMSZf8tU1-nh6TB70dIj65_Z6T72_ffLt8X24_vftwebEtnVCQykbzGqmAHlwNTesaLWjPRV_z_EfXVAnaUWxZB5pB23et7mULttcOdKMR-Tl5cZqbK1wtGJPJnRwOg51wXqJhSguhpRbqP9AG8moklxl9fgc9zHkZuchKSQaNAp0pOFEuzDEG7M0x-NGGG8OoWUWZg1lFmVWUYWCyqBx6djt6aUfs_kR-m8nAqxOAeW3XHoOJzuPksPMhOzLd7P89__WduBuyY2eHn3iD8W8PE3PAfF1PZb0UJvORSAX8FwTcuFc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1785128729</pqid></control><display><type>article</type><title>Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><source>ProQuest Central UK/Ireland</source><creator>Long, Huibao, MD ; Xu, Bincan, MM ; Luo, Yanling, MM ; Luo, Keqin, MM</creator><creatorcontrib>Long, Huibao, MD ; Xu, Bincan, MM ; Luo, Yanling, MM ; Luo, Keqin, MM</creatorcontrib><description>Abstract Background NLRP3 inflammasome activation is recently reported to be linked to the pathogenesis of sepsis. Artemisinin is shown to play beneficial effects in sepsis. However, the impacts of artemisinin on burn sepsis have not been investigated. This study is designed to investigate the role of artemisinin in burn sepsis and the involvement of NLRP3 inflammasome activation. Methods Male BALB/c mice were randomly divided into sham burn, burn, burn sepsis, and artemisinin treated groups. Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Adhesion molecules and neutrophil infiltration in lung and heart were detected by real-time polymerase chain reaction. Mortality rates were monitored. Artemisinin was added to Raw 264.7 cells that were stimulated with burn sepsis serum in the presence/absence of an inhibitor of NLRP3 inflammasome, 3, 4-methylenedioxy- β -nitrostyrene. Interleukin (IL) 1 β and IL-18 messenger RNA expression as well as NLRP3 and caspase 1 protein were measured. Results Production of inflammatory cytokines in serum, levels of adhesion molecules and neutrophil infiltration in lung and heart, and mortality rate of burn septic mice were significantly higher than those of control. These effects were attenuated by artemisinin. Artemisinin down-regulated protein levels of NLRP3 and caspase 1 and inhibited the increases of IL-1 β and IL-18 messenger RNA expression from Raw 264.7 cells that were stimulated with burn sepsis serum. These effects of artemisinin were not further strengthened in the presence of 4-methylenedioxy- β -nitrostyrene. Conclusion Artemisinin protects mice from burn sepsis by attenuating the inflammatory response and alleviating inflammatory infiltration in vital organs, likely through inhibiting the activation of NLRP3 inflammasome.</description><identifier>ISSN: 0735-6757</identifier><identifier>EISSN: 1532-8171</identifier><identifier>DOI: 10.1016/j.ajem.2015.12.075</identifier><identifier>PMID: 26830216</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adhesion ; Animals ; Anti-Infective Agents - pharmacology ; Anti-Infective Agents - therapeutic use ; Artemisinins - pharmacology ; Artemisinins - therapeutic use ; Biomarkers - metabolism ; Burns ; Burns - complications ; Carrier Proteins - antagonists & inhibitors ; Carrier Proteins - metabolism ; Cell adhesion & migration ; Cytokines ; Cytokines - metabolism ; Emergency ; Emergency medical care ; Enzyme-Linked Immunosorbent Assay ; Enzymes ; Gene expression ; Infiltration ; Inflammasomes - drug effects ; Inflammasomes - metabolism ; Inflammation ; Kinases ; Laboratory animals ; Male ; Mice ; Mice, Inbred BALB C ; Mortality ; NLR Family, Pyrin Domain-Containing 3 Protein ; Polymerase chain reaction ; Proteins ; Random Allocation ; RAW 264.7 Cells ; Real-Time Polymerase Chain Reaction ; Rodents ; Sepsis ; Sepsis - etiology ; Sepsis - metabolism ; Sepsis - prevention & control ; Studies ; Tumor necrosis factor-TNF</subject><ispartof>The American journal of emergency medicine, 2016-05, Vol.34 (5), p.772-777</ispartof><rights>Elsevier Inc.</rights><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-8936e042f2c628bc8940f34f63893960740d0eb1d2912bfdb9f5b2af9c2989ee3</citedby><cites>FETCH-LOGICAL-c472t-8936e042f2c628bc8940f34f63893960740d0eb1d2912bfdb9f5b2af9c2989ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1785128729?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26830216$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Long, Huibao, MD</creatorcontrib><creatorcontrib>Xu, Bincan, MM</creatorcontrib><creatorcontrib>Luo, Yanling, MM</creatorcontrib><creatorcontrib>Luo, Keqin, MM</creatorcontrib><title>Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation</title><title>The American journal of emergency medicine</title><addtitle>Am J Emerg Med</addtitle><description>Abstract Background NLRP3 inflammasome activation is recently reported to be linked to the pathogenesis of sepsis. Artemisinin is shown to play beneficial effects in sepsis. However, the impacts of artemisinin on burn sepsis have not been investigated. This study is designed to investigate the role of artemisinin in burn sepsis and the involvement of NLRP3 inflammasome activation. Methods Male BALB/c mice were randomly divided into sham burn, burn, burn sepsis, and artemisinin treated groups. Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Adhesion molecules and neutrophil infiltration in lung and heart were detected by real-time polymerase chain reaction. Mortality rates were monitored. Artemisinin was added to Raw 264.7 cells that were stimulated with burn sepsis serum in the presence/absence of an inhibitor of NLRP3 inflammasome, 3, 4-methylenedioxy- β -nitrostyrene. Interleukin (IL) 1 β and IL-18 messenger RNA expression as well as NLRP3 and caspase 1 protein were measured. Results Production of inflammatory cytokines in serum, levels of adhesion molecules and neutrophil infiltration in lung and heart, and mortality rate of burn septic mice were significantly higher than those of control. These effects were attenuated by artemisinin. Artemisinin down-regulated protein levels of NLRP3 and caspase 1 and inhibited the increases of IL-1 β and IL-18 messenger RNA expression from Raw 264.7 cells that were stimulated with burn sepsis serum. These effects of artemisinin were not further strengthened in the presence of 4-methylenedioxy- β -nitrostyrene. Conclusion Artemisinin protects mice from burn sepsis by attenuating the inflammatory response and alleviating inflammatory infiltration in vital organs, likely through inhibiting the activation of NLRP3 inflammasome.</description><subject>Adhesion</subject><subject>Animals</subject><subject>Anti-Infective Agents - pharmacology</subject><subject>Anti-Infective Agents - therapeutic use</subject><subject>Artemisinins - pharmacology</subject><subject>Artemisinins - therapeutic use</subject><subject>Biomarkers - metabolism</subject><subject>Burns</subject><subject>Burns - complications</subject><subject>Carrier Proteins - antagonists & inhibitors</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Emergency</subject><subject>Emergency medical care</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Infiltration</subject><subject>Inflammasomes - drug effects</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mortality</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Random Allocation</subject><subject>RAW 264.7 Cells</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Sepsis - etiology</subject><subject>Sepsis - metabolism</subject><subject>Sepsis - prevention & control</subject><subject>Studies</subject><subject>Tumor necrosis factor-TNF</subject><issn>0735-6757</issn><issn>1532-8171</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkl2L1DAUhoMo7rj6B7yQgjfetCYnSdOACMviFwwqftwa0vR0JmM_ZpN0Yf-9KbMq7IV4VUif98B7nkPIU0YrRln98lDZA44VUCYrBhVV8h7ZMMmhbJhi98mGKi7LWkl1Rh7FeKCUMSHFQ3IGdcMpsHpDflyEhKOPfvJTcQxzQpdiMXqHhd1ZP8VUtEuYiojH6GOR9mFedvvCT3vf-uSnXfFx--Uzzw_9YMfRxnnMSZf8tU1-nh6TB70dIj65_Z6T72_ffLt8X24_vftwebEtnVCQykbzGqmAHlwNTesaLWjPRV_z_EfXVAnaUWxZB5pB23et7mULttcOdKMR-Tl5cZqbK1wtGJPJnRwOg51wXqJhSguhpRbqP9AG8moklxl9fgc9zHkZuchKSQaNAp0pOFEuzDEG7M0x-NGGG8OoWUWZg1lFmVWUYWCyqBx6djt6aUfs_kR-m8nAqxOAeW3XHoOJzuPksPMhOzLd7P89__WduBuyY2eHn3iD8W8PE3PAfF1PZb0UJvORSAX8FwTcuFc</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Long, Huibao, MD</creator><creator>Xu, Bincan, MM</creator><creator>Luo, Yanling, MM</creator><creator>Luo, Keqin, MM</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>20160501</creationdate><title>Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation</title><author>Long, Huibao, MD ; Xu, Bincan, MM ; Luo, Yanling, MM ; Luo, Keqin, MM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-8936e042f2c628bc8940f34f63893960740d0eb1d2912bfdb9f5b2af9c2989ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adhesion</topic><topic>Animals</topic><topic>Anti-Infective Agents - pharmacology</topic><topic>Anti-Infective Agents - therapeutic use</topic><topic>Artemisinins - pharmacology</topic><topic>Artemisinins - therapeutic use</topic><topic>Biomarkers - metabolism</topic><topic>Burns</topic><topic>Burns - complications</topic><topic>Carrier Proteins - antagonists & inhibitors</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Emergency</topic><topic>Emergency medical care</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Infiltration</topic><topic>Inflammasomes - drug effects</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mortality</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Random Allocation</topic><topic>RAW 264.7 Cells</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Rodents</topic><topic>Sepsis</topic><topic>Sepsis - etiology</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - prevention & control</topic><topic>Studies</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Long, Huibao, MD</creatorcontrib><creatorcontrib>Xu, Bincan, MM</creatorcontrib><creatorcontrib>Luo, Yanling, MM</creatorcontrib><creatorcontrib>Luo, Keqin, MM</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>The American journal of emergency medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Long, Huibao, MD</au><au>Xu, Bincan, MM</au><au>Luo, Yanling, MM</au><au>Luo, Keqin, MM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation</atitle><jtitle>The American journal of emergency medicine</jtitle><addtitle>Am J Emerg Med</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>34</volume><issue>5</issue><spage>772</spage><epage>777</epage><pages>772-777</pages><issn>0735-6757</issn><eissn>1532-8171</eissn><abstract>Abstract Background NLRP3 inflammasome activation is recently reported to be linked to the pathogenesis of sepsis. Artemisinin is shown to play beneficial effects in sepsis. However, the impacts of artemisinin on burn sepsis have not been investigated. This study is designed to investigate the role of artemisinin in burn sepsis and the involvement of NLRP3 inflammasome activation. Methods Male BALB/c mice were randomly divided into sham burn, burn, burn sepsis, and artemisinin treated groups. Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Adhesion molecules and neutrophil infiltration in lung and heart were detected by real-time polymerase chain reaction. Mortality rates were monitored. Artemisinin was added to Raw 264.7 cells that were stimulated with burn sepsis serum in the presence/absence of an inhibitor of NLRP3 inflammasome, 3, 4-methylenedioxy- β -nitrostyrene. Interleukin (IL) 1 β and IL-18 messenger RNA expression as well as NLRP3 and caspase 1 protein were measured. Results Production of inflammatory cytokines in serum, levels of adhesion molecules and neutrophil infiltration in lung and heart, and mortality rate of burn septic mice were significantly higher than those of control. These effects were attenuated by artemisinin. Artemisinin down-regulated protein levels of NLRP3 and caspase 1 and inhibited the increases of IL-1 β and IL-18 messenger RNA expression from Raw 264.7 cells that were stimulated with burn sepsis serum. These effects of artemisinin were not further strengthened in the presence of 4-methylenedioxy- β -nitrostyrene. Conclusion Artemisinin protects mice from burn sepsis by attenuating the inflammatory response and alleviating inflammatory infiltration in vital organs, likely through inhibiting the activation of NLRP3 inflammasome.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26830216</pmid><doi>10.1016/j.ajem.2015.12.075</doi><tpages>6</tpages></addata></record> |
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| subjects | Adhesion Animals Anti-Infective Agents - pharmacology Anti-Infective Agents - therapeutic use Artemisinins - pharmacology Artemisinins - therapeutic use Biomarkers - metabolism Burns Burns - complications Carrier Proteins - antagonists & inhibitors Carrier Proteins - metabolism Cell adhesion & migration Cytokines Cytokines - metabolism Emergency Emergency medical care Enzyme-Linked Immunosorbent Assay Enzymes Gene expression Infiltration Inflammasomes - drug effects Inflammasomes - metabolism Inflammation Kinases Laboratory animals Male Mice Mice, Inbred BALB C Mortality NLR Family, Pyrin Domain-Containing 3 Protein Polymerase chain reaction Proteins Random Allocation RAW 264.7 Cells Real-Time Polymerase Chain Reaction Rodents Sepsis Sepsis - etiology Sepsis - metabolism Sepsis - prevention & control Studies Tumor necrosis factor-TNF |
| title | Artemisinin protects mice against burn sepsis through inhibiting NLRP3 inflammasome activation |
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