Electroacupuncture preconditioning attenuates acute myocardial ischemia injury through inhibiting NLRP3 inflammasome activation in mice
Electro-acupuncture pretreatment (EAP) plays a protective role in myocardial ischemia (MI) injury. However, the underlying mechanism remains unclear. A growing body of evidence suggests postinfarction inflammatory response directly affects the remodeling of ventricular function. The purpose of this...
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Veröffentlicht in: | Life sciences (1973) 2020-05, Vol.248, p.117451-10, Article 117451 |
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creator | Zhang, Tao Yang, Wen-xiu Wang, Ya-ling Yuan, Jing Qian, Yi Sun, Qin-mei Yu, Mei-ling Fu, Shu-ping Xu, Bin Lu, Sheng-feng |
description | Electro-acupuncture pretreatment (EAP) plays a protective role in myocardial ischemia (MI) injury. However, the underlying mechanism remains unclear. A growing body of evidence suggests postinfarction inflammatory response directly affects the remodeling of ventricular function. The purpose of this study was to investigate whether EAP alleviates MI through NLRP3 inflammasome inhibition.
We constructed an AMI model by ligating the left anterior descending (LAD) coronary artery after 3 days of EAP with C57BL/6 mice. Echocardiography and TTC staining were employed to evaluate cardiac function and infarct size after 24 h of ischemia. HE staining and immunohistochemistry were employed to determine inflammatory level. Then, inflammasome activation was detected by western blotting, and macrophage polarization and neutrophil infiltration were observed by flow cytometry.
Our preliminary findings showed that EAP reduced the infarct area and increased fractional shortening (FS) and ejection fraction (EF) and decreased the degree of inflammation after AMI injury. Meanwhile, EAP inhibited the expression of NLRP3, cleaved caspase-1 and IL-1β in ischemia myocardial tissue, companied by inhibiting the expression of F4/80+, CD11b+, CD206low macrophages and activated M2 macrophage, and decreasing Ly-6G+CD11b+ neutrophils in ischemia myocardial and spleen tissue.
EAP inhibits the activation of NLRP3 inflammasome, promotes M2 polarization of macrophages and reduces the recruitment of neutrophils in damaged myocardium, thereby decreases the infarct size and improves the cardiac function. |
doi_str_mv | 10.1016/j.lfs.2020.117451 |
format | Article |
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We constructed an AMI model by ligating the left anterior descending (LAD) coronary artery after 3 days of EAP with C57BL/6 mice. Echocardiography and TTC staining were employed to evaluate cardiac function and infarct size after 24 h of ischemia. HE staining and immunohistochemistry were employed to determine inflammatory level. Then, inflammasome activation was detected by western blotting, and macrophage polarization and neutrophil infiltration were observed by flow cytometry.
Our preliminary findings showed that EAP reduced the infarct area and increased fractional shortening (FS) and ejection fraction (EF) and decreased the degree of inflammation after AMI injury. Meanwhile, EAP inhibited the expression of NLRP3, cleaved caspase-1 and IL-1β in ischemia myocardial tissue, companied by inhibiting the expression of F4/80+, CD11b+, CD206low macrophages and activated M2 macrophage, and decreasing Ly-6G+CD11b+ neutrophils in ischemia myocardial and spleen tissue.
EAP inhibits the activation of NLRP3 inflammasome, promotes M2 polarization of macrophages and reduces the recruitment of neutrophils in damaged myocardium, thereby decreases the infarct size and improves the cardiac function.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.117451</identifier><identifier>PMID: 32088213</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Activation ; Acupuncture ; Animals ; Antigens, Ly - genetics ; Antigens, Ly - immunology ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - immunology ; Cardiac function ; Cardioprotection ; Caspase 1 - genetics ; Caspase 1 - immunology ; Caspase-1 ; CD11b antigen ; CD11b Antigen - genetics ; CD11b Antigen - immunology ; Coronary artery ; Disease Models, Animal ; Echocardiography ; Electro-acupuncture preconditioning ; Electroacupuncture - methods ; Flow cytometry ; Gene Expression Regulation ; Heart ; IL-1β ; Immunohistochemistry ; Inflammasomes ; Inflammasomes - genetics ; Inflammasomes - immunology ; Inflammation ; Inflammatory response ; Injuries ; Interleukin-1beta - genetics ; Interleukin-1beta - immunology ; Ischemia ; Ischemic Preconditioning, Myocardial ; Lectins, C-Type - genetics ; Lectins, C-Type - immunology ; Leukocytes (neutrophilic) ; Ly-6 antigen ; M2 macrophage polarization ; Macrophages ; Macrophages - immunology ; Macrophages - pathology ; Male ; Mannose-Binding Lectins - genetics ; Mannose-Binding Lectins - immunology ; Mice ; Mice, Inbred C57BL ; Myocardial ischemia ; Myocardial Ischemia - genetics ; Myocardial Ischemia - immunology ; Myocardial Ischemia - pathology ; Myocardial Ischemia - therapy ; Myocardial ischemic injury ; Myocardium ; Myocardium - immunology ; Myocardium - pathology ; Neutrophil Infiltration ; Neutrophils ; Neutrophils - immunology ; Neutrophils - pathology ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - immunology ; NLRP3 inflammasome inhibition ; Polarization ; Preconditioning ; Pretreatment ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - immunology ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - immunology ; Signal Transduction ; Spleen ; Staining ; Ventricle ; Western blotting</subject><ispartof>Life sciences (1973), 2020-05, Vol.248, p.117451-10, Article 117451</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV May 1, 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-85778037e2b92df3289a7af334dbf086001a428674e25d35d07f37d67c8519d43</citedby><cites>FETCH-LOGICAL-c447t-85778037e2b92df3289a7af334dbf086001a428674e25d35d07f37d67c8519d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320520301995$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32088213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Tao</creatorcontrib><creatorcontrib>Yang, Wen-xiu</creatorcontrib><creatorcontrib>Wang, Ya-ling</creatorcontrib><creatorcontrib>Yuan, Jing</creatorcontrib><creatorcontrib>Qian, Yi</creatorcontrib><creatorcontrib>Sun, Qin-mei</creatorcontrib><creatorcontrib>Yu, Mei-ling</creatorcontrib><creatorcontrib>Fu, Shu-ping</creatorcontrib><creatorcontrib>Xu, Bin</creatorcontrib><creatorcontrib>Lu, Sheng-feng</creatorcontrib><title>Electroacupuncture preconditioning attenuates acute myocardial ischemia injury through inhibiting NLRP3 inflammasome activation in mice</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Electro-acupuncture pretreatment (EAP) plays a protective role in myocardial ischemia (MI) injury. However, the underlying mechanism remains unclear. A growing body of evidence suggests postinfarction inflammatory response directly affects the remodeling of ventricular function. The purpose of this study was to investigate whether EAP alleviates MI through NLRP3 inflammasome inhibition.
We constructed an AMI model by ligating the left anterior descending (LAD) coronary artery after 3 days of EAP with C57BL/6 mice. Echocardiography and TTC staining were employed to evaluate cardiac function and infarct size after 24 h of ischemia. HE staining and immunohistochemistry were employed to determine inflammatory level. Then, inflammasome activation was detected by western blotting, and macrophage polarization and neutrophil infiltration were observed by flow cytometry.
Our preliminary findings showed that EAP reduced the infarct area and increased fractional shortening (FS) and ejection fraction (EF) and decreased the degree of inflammation after AMI injury. Meanwhile, EAP inhibited the expression of NLRP3, cleaved caspase-1 and IL-1β in ischemia myocardial tissue, companied by inhibiting the expression of F4/80+, CD11b+, CD206low macrophages and activated M2 macrophage, and decreasing Ly-6G+CD11b+ neutrophils in ischemia myocardial and spleen tissue.
EAP inhibits the activation of NLRP3 inflammasome, promotes M2 polarization of macrophages and reduces the recruitment of neutrophils in damaged myocardium, thereby decreases the infarct size and improves the cardiac function.</description><subject>Activation</subject><subject>Acupuncture</subject><subject>Animals</subject><subject>Antigens, Ly - genetics</subject><subject>Antigens, Ly - immunology</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - immunology</subject><subject>Cardiac function</subject><subject>Cardioprotection</subject><subject>Caspase 1 - genetics</subject><subject>Caspase 1 - immunology</subject><subject>Caspase-1</subject><subject>CD11b antigen</subject><subject>CD11b Antigen - genetics</subject><subject>CD11b Antigen - immunology</subject><subject>Coronary artery</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Electro-acupuncture preconditioning</subject><subject>Electroacupuncture - methods</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation</subject><subject>Heart</subject><subject>IL-1β</subject><subject>Immunohistochemistry</subject><subject>Inflammasomes</subject><subject>Inflammasomes - genetics</subject><subject>Inflammasomes - immunology</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - immunology</subject><subject>Ischemia</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>Lectins, C-Type - genetics</subject><subject>Lectins, C-Type - immunology</subject><subject>Leukocytes (neutrophilic)</subject><subject>Ly-6 antigen</subject><subject>M2 macrophage polarization</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Mannose-Binding Lectins - genetics</subject><subject>Mannose-Binding Lectins - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial ischemia</subject><subject>Myocardial Ischemia - genetics</subject><subject>Myocardial Ischemia - immunology</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - therapy</subject><subject>Myocardial ischemic injury</subject><subject>Myocardium</subject><subject>Myocardium - immunology</subject><subject>Myocardium - pathology</subject><subject>Neutrophil Infiltration</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - pathology</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - immunology</subject><subject>NLRP3 inflammasome inhibition</subject><subject>Polarization</subject><subject>Preconditioning</subject><subject>Pretreatment</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - immunology</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - immunology</subject><subject>Signal Transduction</subject><subject>Spleen</subject><subject>Staining</subject><subject>Ventricle</subject><subject>Western blotting</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1rFDEYx4Modlv9AF5kwEsvs-Z1ksGTlGqFxRbRc8gmz3QzzEzWvBT2E_RrN8tWDx48hefh9_-R5I_QO4LXBJPu47iehrSmmNaZSC7IC7QiSvYt7hh5iVYYU94yisUZOk9pxBgLIdlrdFZ3SlHCVujxegKbYzC27Mtic4nQ7CPYsDiffVj8ct-YnGEpJkNqKpahmQ_Bmui8mRqf7A5mbxq_jCUemryLodzv6rjz22qo8e-bH3esLobJzLNJYYaqyf7BHP1138zewhv0ajBTgrfP5wX69eX659VNu7n9-u3q86a1nMvcKiGlwkwC3fbUDYyq3kgzMMbddsCqw5gYTlUnOVDhmHBYDky6TlolSO84u0CXJ-8-ht8FUtZzfQJMk1kglKQp6xhWUnJa0Q__oGMocam305QTiYnouagUOVE2hpQiDHof_WziQROsjy3pUdeW9LElfWqpZt4_m8t2Bvc38aeWCnw6AVC_4sFD1Ml6WCw4X7vJ2gX_H_0TKYaj6w</recordid><startdate>20200501</startdate><enddate>20200501</enddate><creator>Zhang, Tao</creator><creator>Yang, Wen-xiu</creator><creator>Wang, Ya-ling</creator><creator>Yuan, Jing</creator><creator>Qian, Yi</creator><creator>Sun, Qin-mei</creator><creator>Yu, Mei-ling</creator><creator>Fu, Shu-ping</creator><creator>Xu, Bin</creator><creator>Lu, Sheng-feng</creator><general>Elsevier Inc</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20200501</creationdate><title>Electroacupuncture preconditioning attenuates acute myocardial ischemia injury through inhibiting NLRP3 inflammasome activation in mice</title><author>Zhang, Tao ; Yang, Wen-xiu ; Wang, Ya-ling ; Yuan, Jing ; Qian, Yi ; Sun, Qin-mei ; Yu, Mei-ling ; Fu, Shu-ping ; Xu, Bin ; Lu, Sheng-feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-85778037e2b92df3289a7af334dbf086001a428674e25d35d07f37d67c8519d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Activation</topic><topic>Acupuncture</topic><topic>Animals</topic><topic>Antigens, Ly - genetics</topic><topic>Antigens, Ly - immunology</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - immunology</topic><topic>Cardiac function</topic><topic>Cardioprotection</topic><topic>Caspase 1 - genetics</topic><topic>Caspase 1 - immunology</topic><topic>Caspase-1</topic><topic>CD11b antigen</topic><topic>CD11b Antigen - genetics</topic><topic>CD11b Antigen - immunology</topic><topic>Coronary artery</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Electro-acupuncture preconditioning</topic><topic>Electroacupuncture - methods</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation</topic><topic>Heart</topic><topic>IL-1β</topic><topic>Immunohistochemistry</topic><topic>Inflammasomes</topic><topic>Inflammasomes - genetics</topic><topic>Inflammasomes - immunology</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - immunology</topic><topic>Ischemia</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>Lectins, C-Type - genetics</topic><topic>Lectins, C-Type - immunology</topic><topic>Leukocytes (neutrophilic)</topic><topic>Ly-6 antigen</topic><topic>M2 macrophage polarization</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Mannose-Binding Lectins - genetics</topic><topic>Mannose-Binding Lectins - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardial ischemia</topic><topic>Myocardial Ischemia - genetics</topic><topic>Myocardial Ischemia - immunology</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Ischemia - therapy</topic><topic>Myocardial ischemic injury</topic><topic>Myocardium</topic><topic>Myocardium - immunology</topic><topic>Myocardium - pathology</topic><topic>Neutrophil Infiltration</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - pathology</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - immunology</topic><topic>NLRP3 inflammasome inhibition</topic><topic>Polarization</topic><topic>Preconditioning</topic><topic>Pretreatment</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - immunology</topic><topic>Receptors, G-Protein-Coupled - genetics</topic><topic>Receptors, G-Protein-Coupled - immunology</topic><topic>Signal Transduction</topic><topic>Spleen</topic><topic>Staining</topic><topic>Ventricle</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Tao</creatorcontrib><creatorcontrib>Yang, Wen-xiu</creatorcontrib><creatorcontrib>Wang, Ya-ling</creatorcontrib><creatorcontrib>Yuan, Jing</creatorcontrib><creatorcontrib>Qian, Yi</creatorcontrib><creatorcontrib>Sun, Qin-mei</creatorcontrib><creatorcontrib>Yu, Mei-ling</creatorcontrib><creatorcontrib>Fu, Shu-ping</creatorcontrib><creatorcontrib>Xu, Bin</creatorcontrib><creatorcontrib>Lu, Sheng-feng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences 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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Tao</au><au>Yang, Wen-xiu</au><au>Wang, Ya-ling</au><au>Yuan, Jing</au><au>Qian, Yi</au><au>Sun, Qin-mei</au><au>Yu, Mei-ling</au><au>Fu, Shu-ping</au><au>Xu, Bin</au><au>Lu, Sheng-feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroacupuncture preconditioning attenuates acute myocardial ischemia injury through inhibiting NLRP3 inflammasome activation in mice</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2020-05-01</date><risdate>2020</risdate><volume>248</volume><spage>117451</spage><epage>10</epage><pages>117451-10</pages><artnum>117451</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Electro-acupuncture pretreatment (EAP) plays a protective role in myocardial ischemia (MI) injury. However, the underlying mechanism remains unclear. A growing body of evidence suggests postinfarction inflammatory response directly affects the remodeling of ventricular function. The purpose of this study was to investigate whether EAP alleviates MI through NLRP3 inflammasome inhibition.
We constructed an AMI model by ligating the left anterior descending (LAD) coronary artery after 3 days of EAP with C57BL/6 mice. Echocardiography and TTC staining were employed to evaluate cardiac function and infarct size after 24 h of ischemia. HE staining and immunohistochemistry were employed to determine inflammatory level. Then, inflammasome activation was detected by western blotting, and macrophage polarization and neutrophil infiltration were observed by flow cytometry.
Our preliminary findings showed that EAP reduced the infarct area and increased fractional shortening (FS) and ejection fraction (EF) and decreased the degree of inflammation after AMI injury. Meanwhile, EAP inhibited the expression of NLRP3, cleaved caspase-1 and IL-1β in ischemia myocardial tissue, companied by inhibiting the expression of F4/80+, CD11b+, CD206low macrophages and activated M2 macrophage, and decreasing Ly-6G+CD11b+ neutrophils in ischemia myocardial and spleen tissue.
EAP inhibits the activation of NLRP3 inflammasome, promotes M2 polarization of macrophages and reduces the recruitment of neutrophils in damaged myocardium, thereby decreases the infarct size and improves the cardiac function.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>32088213</pmid><doi>10.1016/j.lfs.2020.117451</doi><tpages>10</tpages></addata></record> |
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subjects | Activation Acupuncture Animals Antigens, Ly - genetics Antigens, Ly - immunology Calcium-Binding Proteins - genetics Calcium-Binding Proteins - immunology Cardiac function Cardioprotection Caspase 1 - genetics Caspase 1 - immunology Caspase-1 CD11b antigen CD11b Antigen - genetics CD11b Antigen - immunology Coronary artery Disease Models, Animal Echocardiography Electro-acupuncture preconditioning Electroacupuncture - methods Flow cytometry Gene Expression Regulation Heart IL-1β Immunohistochemistry Inflammasomes Inflammasomes - genetics Inflammasomes - immunology Inflammation Inflammatory response Injuries Interleukin-1beta - genetics Interleukin-1beta - immunology Ischemia Ischemic Preconditioning, Myocardial Lectins, C-Type - genetics Lectins, C-Type - immunology Leukocytes (neutrophilic) Ly-6 antigen M2 macrophage polarization Macrophages Macrophages - immunology Macrophages - pathology Male Mannose-Binding Lectins - genetics Mannose-Binding Lectins - immunology Mice Mice, Inbred C57BL Myocardial ischemia Myocardial Ischemia - genetics Myocardial Ischemia - immunology Myocardial Ischemia - pathology Myocardial Ischemia - therapy Myocardial ischemic injury Myocardium Myocardium - immunology Myocardium - pathology Neutrophil Infiltration Neutrophils Neutrophils - immunology Neutrophils - pathology NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - immunology NLRP3 inflammasome inhibition Polarization Preconditioning Pretreatment Receptors, Cell Surface - genetics Receptors, Cell Surface - immunology Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - immunology Signal Transduction Spleen Staining Ventricle Western blotting |
title | Electroacupuncture preconditioning attenuates acute myocardial ischemia injury through inhibiting NLRP3 inflammasome activation in mice |
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