Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis
Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed. Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bc...
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description | Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed. Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats. Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis. Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h. Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia. |
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fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5075311</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A610316873</galeid><sourcerecordid>A610316873</sourcerecordid><originalsourceid>FETCH-LOGICAL-c602t-90b66423e37aa833af1fc259fc84c558fda8c14f3441c6b09453651b0f91009c3</originalsourceid><addsrcrecordid>eNqN0tGLFCEcB_Ahiu5u663nGOglqOl01NF5CYblrhYOgqOgN3Hcn7suszrpWOx_n8Nue9XT-aLoh6_641cUrzD6gDFj1zXCzTWvW05r9qS4xJziitZCPD2v-feL4irGHUJZcf68uKi5QHmQy2K4GUBPwSudxuT0lAKU3R4G64OaIJZLCNAHNZSrqLewt6q6hxGCSdF6V67cLoVD2R_Ke9ikQU3zpjdllyY_btXmUCq3LrvRj5OPNr4onhk1RHh5mhfFt9ubr8vP1d2XT6tld1fpBtVT1aK-aWhNgHClBCHKYKNr1hotqGZMmLUSGlNDKMW66VFLGWkY7pFpMUKtJovi4zF3TP0e1hrclL8gx2D3KhykV1b-e-LsVm78T8kQZwTjHPD2FBD8jwRxknsbNQyDcuBTlFgQToig7FGU5Uqjhmf65j-68ym4XIlZUSowa8WD2qgBpHXG5yfqOVR2DUYENyLfvSjeH5UOPsYA5vw7jOTcF3LuC3nqi8xf_12RM_7TCBm8O4KtdWv1yz4yDrIBox40RpSQlvwGRYLJcA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1834481598</pqid></control><display><type>article</type><title>Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Zhou, Shuang ; Qian, Xiao-Lu ; You, Yan-Li ; Li, Chun-Ming ; Shu, Shi ; Ling, Chang-Quan</creator><contributor>Su, Shan-Yu</contributor><creatorcontrib>Zhou, Shuang ; Qian, Xiao-Lu ; You, Yan-Li ; Li, Chun-Ming ; Shu, Shi ; Ling, Chang-Quan ; Su, Shan-Yu</creatorcontrib><description>Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed. Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats. Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis. Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h. Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2016/7297425</identifier><identifier>PMID: 27800003</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Acupuncture ; Analysis ; Apoptosis ; Autophagy ; Carotid arteries ; Cerebral ischemia ; Chinese medicine ; Experiments ; Health aspects ; Ischemia ; Laboratory animals ; Proteins ; Rodents ; Stroke</subject><ispartof>Evidence-based complementary and alternative medicine, 2016-01, Vol.2016 (2016), p.1-8</ispartof><rights>Copyright © 2016 Shi Shu et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Shi Shu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 Shi Shu et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c602t-90b66423e37aa833af1fc259fc84c558fda8c14f3441c6b09453651b0f91009c3</citedby><cites>FETCH-LOGICAL-c602t-90b66423e37aa833af1fc259fc84c558fda8c14f3441c6b09453651b0f91009c3</cites><orcidid>0000-0002-3773-8127 ; 0000-0003-1756-8519</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075311/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075311/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27800003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Su, Shan-Yu</contributor><creatorcontrib>Zhou, Shuang</creatorcontrib><creatorcontrib>Qian, Xiao-Lu</creatorcontrib><creatorcontrib>You, Yan-Li</creatorcontrib><creatorcontrib>Li, Chun-Ming</creatorcontrib><creatorcontrib>Shu, Shi</creatorcontrib><creatorcontrib>Ling, Chang-Quan</creatorcontrib><title>Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed. Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats. Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis. Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h. Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia.</description><subject>Acupuncture</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Carotid arteries</subject><subject>Cerebral ischemia</subject><subject>Chinese medicine</subject><subject>Experiments</subject><subject>Health aspects</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Stroke</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</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>eNqN0tGLFCEcB_Ahiu5u663nGOglqOl01NF5CYblrhYOgqOgN3Hcn7suszrpWOx_n8Nue9XT-aLoh6_641cUrzD6gDFj1zXCzTWvW05r9qS4xJziitZCPD2v-feL4irGHUJZcf68uKi5QHmQy2K4GUBPwSudxuT0lAKU3R4G64OaIJZLCNAHNZSrqLewt6q6hxGCSdF6V67cLoVD2R_Ke9ikQU3zpjdllyY_btXmUCq3LrvRj5OPNr4onhk1RHh5mhfFt9ubr8vP1d2XT6tld1fpBtVT1aK-aWhNgHClBCHKYKNr1hotqGZMmLUSGlNDKMW66VFLGWkY7pFpMUKtJovi4zF3TP0e1hrclL8gx2D3KhykV1b-e-LsVm78T8kQZwTjHPD2FBD8jwRxknsbNQyDcuBTlFgQToig7FGU5Uqjhmf65j-68ym4XIlZUSowa8WD2qgBpHXG5yfqOVR2DUYENyLfvSjeH5UOPsYA5vw7jOTcF3LuC3nqi8xf_12RM_7TCBm8O4KtdWv1yz4yDrIBox40RpSQlvwGRYLJcA</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Zhou, Shuang</creator><creator>Qian, Xiao-Lu</creator><creator>You, Yan-Li</creator><creator>Li, Chun-Ming</creator><creator>Shu, Shi</creator><creator>Ling, Chang-Quan</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</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>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3773-8127</orcidid><orcidid>https://orcid.org/0000-0003-1756-8519</orcidid></search><sort><creationdate>20160101</creationdate><title>Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis</title><author>Zhou, Shuang ; Qian, Xiao-Lu ; You, Yan-Li ; Li, Chun-Ming ; Shu, Shi ; Ling, Chang-Quan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c602t-90b66423e37aa833af1fc259fc84c558fda8c14f3441c6b09453651b0f91009c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acupuncture</topic><topic>Analysis</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Carotid arteries</topic><topic>Cerebral ischemia</topic><topic>Chinese medicine</topic><topic>Experiments</topic><topic>Health aspects</topic><topic>Ischemia</topic><topic>Laboratory animals</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Shuang</creatorcontrib><creatorcontrib>Qian, Xiao-Lu</creatorcontrib><creatorcontrib>You, Yan-Li</creatorcontrib><creatorcontrib>Li, Chun-Ming</creatorcontrib><creatorcontrib>Shu, Shi</creatorcontrib><creatorcontrib>Ling, Chang-Quan</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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>Psychology Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content 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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Evidence-based complementary and alternative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Shuang</au><au>Qian, Xiao-Lu</au><au>You, Yan-Li</au><au>Li, Chun-Ming</au><au>Shu, Shi</au><au>Ling, Chang-Quan</au><au>Su, Shan-Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><addtitle>Evid Based Complement Alternat Med</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>2016</volume><issue>2016</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed. Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats. Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis. Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h. Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>27800003</pmid><doi>10.1155/2016/7297425</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-3773-8127</orcidid><orcidid>https://orcid.org/0000-0003-1756-8519</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acupuncture Analysis Apoptosis Autophagy Carotid arteries Cerebral ischemia Chinese medicine Experiments Health aspects Ischemia Laboratory animals Proteins Rodents Stroke |
title | Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis |
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