Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation
Background/Aims: Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mous...
Gespeichert in:
| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.49 (5), p.1918-1932 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1932 |
|---|---|
| container_issue | 5 |
| container_start_page | 1918 |
| container_title | Cellular physiology and biochemistry |
| container_volume | 49 |
| creator | Zhang, Hailin Chen, Sha Zeng, Meichun Lin, Daopeng Wang, Yu Wen, Xunhang Xu, Changfu Yang, Li Fan, Xiaofang Gong, Yongsheng Zhang, Hongyu Kong, Xiaoxia |
| description | Background/Aims: Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mouse lung injury model and a cell model were designed to explore the mechanism of how apelin-13 alleviates the acute lung injury caused by LPS. Methods: The effect of apelin-13 on LPS-induced structural damage was determined by H&E staining and by the wet/dry weight ratio. The related inflammatory factors in BALF were examined by ELISA. The apoptotic pathway and the NF-κB and NLRP3 inflammasome pathways were evaluated by using Western blotting and immunofluorescence staining. Results: LPS induced the structural damage and the production of inflammatory cytokines in the lung tissues of mice. These deleterious effects were attenuated by apelin-13 administration. The protective effects of apelin-13 were associated with decreased reactive oxygen species (ROS) formation and the inhibition of the activation of the NF-κB and NLRP3 inflammasome pathways in mice and in Raw264.7 cells. Conclusion: Taken together, these data suggest that apelin-13 administration ameliorates LPS-induced acute lung injury by suppressing ROS formation, as well as by inhibiting the NF-κB pathway and the activation of the NLRP3 inflammasome in the lungs. |
| doi_str_mv | 10.1159/000493653 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_karge</sourceid><recordid>TN_cdi_karger_primary_493653</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_20f790c1a2be45558a1bde772ecb0906</doaj_id><sourcerecordid>2301887853</sourcerecordid><originalsourceid>FETCH-LOGICAL-c463t-cec25cb24672c543946e48e079d0b22a0231a81d7ba981096e2080afdfacf8563</originalsourceid><addsrcrecordid>eNptkUtuFDEQhlsIREJgwR4hS9nAosGPdttedkYERhqFEY-1VW27Jx76MbHdoLkAh-IQnAknE2aB8KbK5a9-V-kviucEvyGEq7cY40qxmrMHxSmpKCmVEPJhzjHhpVRSnBRPYtzifBWKPi5OGKaMV5ycFj-bnev9WBKGGjv40ccUIPlpROswJWdSRM0G_BgTWq0_l8vRzsZZ1Jg5ObSaxw1ajts57FG7z9m1b33yuXh1Wf7-dYHWkK5_wB7BaNHV6tOaZabrYRggToPLKsl_v_vtafGogz66Z_fxrPh6-e7L4kO5-vh-uWhWpalqlkrjDOWmpVUtqOEVU1XtKumwUBa3lEJei4AkVrSgJMGqdhRLDJ3twHSS1-ysWB507QRbvQt-gLDXE3h9V5jCRkNI3vROU9wJhQ0B2rqKcy6BtNYJQZ1pscK3Wq8OWrsw3cwuJj34aFzfw-imOWpK8uFEMZrR83_Q7TSHMW-qKcNESiE5y9TrA2XCFGNw3XFAgvWt0fpodGZf3ivO7eDskfzrbAZeHIBvEDYuHIFj__l_nxfriwOhd7ZjfwDPq7YW</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2301887853</pqid></control><display><type>article</type><title>Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Karger Open Access</source><creator>Zhang, Hailin ; Chen, Sha ; Zeng, Meichun ; Lin, Daopeng ; Wang, Yu ; Wen, Xunhang ; Xu, Changfu ; Yang, Li ; Fan, Xiaofang ; Gong, Yongsheng ; Zhang, Hongyu ; Kong, Xiaoxia</creator><creatorcontrib>Zhang, Hailin ; Chen, Sha ; Zeng, Meichun ; Lin, Daopeng ; Wang, Yu ; Wen, Xunhang ; Xu, Changfu ; Yang, Li ; Fan, Xiaofang ; Gong, Yongsheng ; Zhang, Hongyu ; Kong, Xiaoxia</creatorcontrib><description>Background/Aims: Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mouse lung injury model and a cell model were designed to explore the mechanism of how apelin-13 alleviates the acute lung injury caused by LPS. Methods: The effect of apelin-13 on LPS-induced structural damage was determined by H&E staining and by the wet/dry weight ratio. The related inflammatory factors in BALF were examined by ELISA. The apoptotic pathway and the NF-κB and NLRP3 inflammasome pathways were evaluated by using Western blotting and immunofluorescence staining. Results: LPS induced the structural damage and the production of inflammatory cytokines in the lung tissues of mice. These deleterious effects were attenuated by apelin-13 administration. The protective effects of apelin-13 were associated with decreased reactive oxygen species (ROS) formation and the inhibition of the activation of the NF-κB and NLRP3 inflammasome pathways in mice and in Raw264.7 cells. Conclusion: Taken together, these data suggest that apelin-13 administration ameliorates LPS-induced acute lung injury by suppressing ROS formation, as well as by inhibiting the NF-κB pathway and the activation of the NLRP3 inflammasome in the lungs.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000493653</identifier><identifier>PMID: 30235451</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acute lung injury (ALI) ; Acute Lung Injury - etiology ; Acute Lung Injury - prevention & control ; Animals ; Apelin - pharmacology ; Apelin - therapeutic use ; Apelin-13 ; Apoptosis - drug effects ; Bronchoalveolar Lavage Fluid - chemistry ; Cytokines ; Cytokines - analysis ; Disease Models, Animal ; Inflammasomes - metabolism ; Inflammation ; Lipopolysaccharide (LPS) ; Lipopolysaccharides - toxicity ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lungs ; Male ; Membrane Potential, Mitochondrial - drug effects ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; NF-κB ; Nitric oxide ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 ; Original Paper ; Pathogenesis ; Peptides ; Physiology ; Protective Agents - pharmacology ; Protective Agents - therapeutic use ; Proteins ; RAW 264.7 Cells ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Respiratory distress syndrome ; Sepsis ; Signal Transduction - drug effects ; Tumor necrosis factor-TNF</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.49 (5), p.1918-1932</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-cec25cb24672c543946e48e079d0b22a0231a81d7ba981096e2080afdfacf8563</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2095,27614,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30235451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Hailin</creatorcontrib><creatorcontrib>Chen, Sha</creatorcontrib><creatorcontrib>Zeng, Meichun</creatorcontrib><creatorcontrib>Lin, Daopeng</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Wen, Xunhang</creatorcontrib><creatorcontrib>Xu, Changfu</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Fan, Xiaofang</creatorcontrib><creatorcontrib>Gong, Yongsheng</creatorcontrib><creatorcontrib>Zhang, Hongyu</creatorcontrib><creatorcontrib>Kong, Xiaoxia</creatorcontrib><title>Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mouse lung injury model and a cell model were designed to explore the mechanism of how apelin-13 alleviates the acute lung injury caused by LPS. Methods: The effect of apelin-13 on LPS-induced structural damage was determined by H&E staining and by the wet/dry weight ratio. The related inflammatory factors in BALF were examined by ELISA. The apoptotic pathway and the NF-κB and NLRP3 inflammasome pathways were evaluated by using Western blotting and immunofluorescence staining. Results: LPS induced the structural damage and the production of inflammatory cytokines in the lung tissues of mice. These deleterious effects were attenuated by apelin-13 administration. The protective effects of apelin-13 were associated with decreased reactive oxygen species (ROS) formation and the inhibition of the activation of the NF-κB and NLRP3 inflammasome pathways in mice and in Raw264.7 cells. Conclusion: Taken together, these data suggest that apelin-13 administration ameliorates LPS-induced acute lung injury by suppressing ROS formation, as well as by inhibiting the NF-κB pathway and the activation of the NLRP3 inflammasome in the lungs.</description><subject>Acute lung injury (ALI)</subject><subject>Acute Lung Injury - etiology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Animals</subject><subject>Apelin - pharmacology</subject><subject>Apelin - therapeutic use</subject><subject>Apelin-13</subject><subject>Apoptosis - drug effects</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Cytokines</subject><subject>Cytokines - analysis</subject><subject>Disease Models, Animal</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Lipopolysaccharide (LPS)</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Male</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>Nitric oxide</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3</subject><subject>Original Paper</subject><subject>Pathogenesis</subject><subject>Peptides</subject><subject>Physiology</subject><subject>Protective Agents - pharmacology</subject><subject>Protective Agents - therapeutic use</subject><subject>Proteins</subject><subject>RAW 264.7 Cells</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Respiratory distress syndrome</subject><subject>Sepsis</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor necrosis factor-TNF</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkUtuFDEQhlsIREJgwR4hS9nAosGPdttedkYERhqFEY-1VW27Jx76MbHdoLkAh-IQnAknE2aB8KbK5a9-V-kviucEvyGEq7cY40qxmrMHxSmpKCmVEPJhzjHhpVRSnBRPYtzifBWKPi5OGKaMV5ycFj-bnev9WBKGGjv40ccUIPlpROswJWdSRM0G_BgTWq0_l8vRzsZZ1Jg5ObSaxw1ajts57FG7z9m1b33yuXh1Wf7-dYHWkK5_wB7BaNHV6tOaZabrYRggToPLKsl_v_vtafGogz66Z_fxrPh6-e7L4kO5-vh-uWhWpalqlkrjDOWmpVUtqOEVU1XtKumwUBa3lEJei4AkVrSgJMGqdhRLDJ3twHSS1-ysWB507QRbvQt-gLDXE3h9V5jCRkNI3vROU9wJhQ0B2rqKcy6BtNYJQZ1pscK3Wq8OWrsw3cwuJj34aFzfw-imOWpK8uFEMZrR83_Q7TSHMW-qKcNESiE5y9TrA2XCFGNw3XFAgvWt0fpodGZf3ivO7eDskfzrbAZeHIBvEDYuHIFj__l_nxfriwOhd7ZjfwDPq7YW</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Zhang, Hailin</creator><creator>Chen, Sha</creator><creator>Zeng, Meichun</creator><creator>Lin, Daopeng</creator><creator>Wang, Yu</creator><creator>Wen, Xunhang</creator><creator>Xu, Changfu</creator><creator>Yang, Li</creator><creator>Fan, Xiaofang</creator><creator>Gong, Yongsheng</creator><creator>Zhang, Hongyu</creator><creator>Kong, Xiaoxia</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation</title><author>Zhang, Hailin ; Chen, Sha ; Zeng, Meichun ; Lin, Daopeng ; Wang, Yu ; Wen, Xunhang ; Xu, Changfu ; Yang, Li ; Fan, Xiaofang ; Gong, Yongsheng ; Zhang, Hongyu ; Kong, Xiaoxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-cec25cb24672c543946e48e079d0b22a0231a81d7ba981096e2080afdfacf8563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acute lung injury (ALI)</topic><topic>Acute Lung Injury - etiology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Animals</topic><topic>Apelin - pharmacology</topic><topic>Apelin - therapeutic use</topic><topic>Apelin-13</topic><topic>Apoptosis - drug effects</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Cytokines</topic><topic>Cytokines - analysis</topic><topic>Disease Models, Animal</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Lipopolysaccharide (LPS)</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Male</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>Nitric oxide</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3</topic><topic>Original Paper</topic><topic>Pathogenesis</topic><topic>Peptides</topic><topic>Physiology</topic><topic>Protective Agents - pharmacology</topic><topic>Protective Agents - therapeutic use</topic><topic>Proteins</topic><topic>RAW 264.7 Cells</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Respiratory distress syndrome</topic><topic>Sepsis</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Hailin</creatorcontrib><creatorcontrib>Chen, Sha</creatorcontrib><creatorcontrib>Zeng, Meichun</creatorcontrib><creatorcontrib>Lin, Daopeng</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Wen, Xunhang</creatorcontrib><creatorcontrib>Xu, Changfu</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Fan, Xiaofang</creatorcontrib><creatorcontrib>Gong, Yongsheng</creatorcontrib><creatorcontrib>Zhang, Hongyu</creatorcontrib><creatorcontrib>Kong, Xiaoxia</creatorcontrib><collection>Karger Open Access</collection><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>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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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 China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Hailin</au><au>Chen, Sha</au><au>Zeng, Meichun</au><au>Lin, Daopeng</au><au>Wang, Yu</au><au>Wen, Xunhang</au><au>Xu, Changfu</au><au>Yang, Li</au><au>Fan, Xiaofang</au><au>Gong, Yongsheng</au><au>Zhang, Hongyu</au><au>Kong, Xiaoxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>49</volume><issue>5</issue><spage>1918</spage><epage>1932</epage><pages>1918-1932</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mouse lung injury model and a cell model were designed to explore the mechanism of how apelin-13 alleviates the acute lung injury caused by LPS. Methods: The effect of apelin-13 on LPS-induced structural damage was determined by H&E staining and by the wet/dry weight ratio. The related inflammatory factors in BALF were examined by ELISA. The apoptotic pathway and the NF-κB and NLRP3 inflammasome pathways were evaluated by using Western blotting and immunofluorescence staining. Results: LPS induced the structural damage and the production of inflammatory cytokines in the lung tissues of mice. These deleterious effects were attenuated by apelin-13 administration. The protective effects of apelin-13 were associated with decreased reactive oxygen species (ROS) formation and the inhibition of the activation of the NF-κB and NLRP3 inflammasome pathways in mice and in Raw264.7 cells. Conclusion: Taken together, these data suggest that apelin-13 administration ameliorates LPS-induced acute lung injury by suppressing ROS formation, as well as by inhibiting the NF-κB pathway and the activation of the NLRP3 inflammasome in the lungs.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30235451</pmid><doi>10.1159/000493653</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1015-8987 |
| ispartof | Cellular physiology and biochemistry, 2018-01, Vol.49 (5), p.1918-1932 |
| issn | 1015-8987 1421-9778 |
| language | eng |
| recordid | cdi_karger_primary_493653 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Karger Open Access |
| subjects | Acute lung injury (ALI) Acute Lung Injury - etiology Acute Lung Injury - prevention & control Animals Apelin - pharmacology Apelin - therapeutic use Apelin-13 Apoptosis - drug effects Bronchoalveolar Lavage Fluid - chemistry Cytokines Cytokines - analysis Disease Models, Animal Inflammasomes - metabolism Inflammation Lipopolysaccharide (LPS) Lipopolysaccharides - toxicity Lung - drug effects Lung - metabolism Lung - pathology Lungs Male Membrane Potential, Mitochondrial - drug effects Mice Mice, Inbred C57BL NF-kappa B - metabolism NF-κB Nitric oxide NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 Original Paper Pathogenesis Peptides Physiology Protective Agents - pharmacology Protective Agents - therapeutic use Proteins RAW 264.7 Cells Reactive oxygen species Reactive Oxygen Species - metabolism Respiratory distress syndrome Sepsis Signal Transduction - drug effects Tumor necrosis factor-TNF |
| title | Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T03%3A36%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_karge&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Apelin-13%20Administration%20Protects%20Against%20LPS-Induced%20Acute%20Lung%20Injury%20by%20Inhibiting%20NF-%CE%BAB%20Pathway%20and%20NLRP3%20Inflammasome%20Activation&rft.jtitle=Cellular%20physiology%20and%20biochemistry&rft.au=Zhang,%20Hailin&rft.date=2018-01-01&rft.volume=49&rft.issue=5&rft.spage=1918&rft.epage=1932&rft.pages=1918-1932&rft.issn=1015-8987&rft.eissn=1421-9778&rft_id=info:doi/10.1159/000493653&rft_dat=%3Cproquest_karge%3E2301887853%3C/proquest_karge%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2301887853&rft_id=info:pmid/30235451&rft_doaj_id=oai_doaj_org_article_20f790c1a2be45558a1bde772ecb0906&rfr_iscdi=true |