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
Hauptverfasser: 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
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container_start_page 117451
container_title Life sciences (1973)
container_volume 248
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.
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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. 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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 - 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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 &amp; 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 - 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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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