Activation of Epsilon Protein Kinase C-Mediated Anti-Apoptosis Is Involved in Rapid Tolerance Induced by Electroacupuncture Pretreatment Through Cannabinoid Receptor Type 1
Our previous study has demonstrated that the rapid tolerance to cerebral ischemia by electroacupuncture (EA) pretreatment was possibly mediated through an endocannabinoid system-related mechanism. The purpose of this study was to investigate whether activation of epsilon protein kinase C (εPKC) was...
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| Veröffentlicht in: | Stroke (1970) 2011-02, Vol.42 (2), p.389-396 |
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| container_title | Stroke (1970) |
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| creator | Wang, Qiang Li, Xuying Chen, Yanke Wang, Feng Yang, Qianzi Chen, Shaoyang Min, Yuyuan Li, Xin Xiong, Lize |
| description | Our previous study has demonstrated that the rapid tolerance to cerebral ischemia by electroacupuncture (EA) pretreatment was possibly mediated through an endocannabinoid system-related mechanism. The purpose of this study was to investigate whether activation of epsilon protein kinase C (εPKC) was involved in EA pretreatment-induced neuroprotection via cannabinoid receptor type 1 in a rat model of transient focal cerebral ischemia.
The activation of εPKC in the ipsilateral brain tissues after EA pretreatment was investigated in the presence or absence of cannabinoid receptor antagonists. At 2 hours after the end of EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 minutes in rats. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the expression of Bcl-2 and Bax were evaluated after reperfusion in the presence or absence of εPKC-selective peptide inhibitor (TAT-εV1-2) or activator (TAT-ψεRACK).
EA pretreatment enhanced εPKC activation. Systemic delivery of TAT-ψεRACK conferred neuroprotection against a subsequent cerebral ischemic event when delivered 2 hours before ischemia. Pretreatment with EA reduced infarct volumes, improved neurological outcome, inhibited neuronal apoptosis, and increased the Bcl-2-to-Bax ratio after reperfusion, and the beneficial effects were attenuated by TAT-εV1-2. In addition, the blockade of cannabinoid receptor type 1, but not cannabinoid receptor type 2 receptor, reversed the increase in εPKC activation and neuroprotection induced by EA pretreatment.
EA pretreatment may activate endogenous εPKC-mediated anti-apoptosis to protect against ischemic damage after focal cerebral ischemia via cannabinoid receptor type 1, which represents a new mechanism of EA pretreatment-induced rapid tolerance to focal cerebral ischemia in rats. |
| doi_str_mv | 10.1161/STROKEAHA.110.597336 |
| format | Article |
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The activation of εPKC in the ipsilateral brain tissues after EA pretreatment was investigated in the presence or absence of cannabinoid receptor antagonists. At 2 hours after the end of EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 minutes in rats. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the expression of Bcl-2 and Bax were evaluated after reperfusion in the presence or absence of εPKC-selective peptide inhibitor (TAT-εV1-2) or activator (TAT-ψεRACK).
EA pretreatment enhanced εPKC activation. Systemic delivery of TAT-ψεRACK conferred neuroprotection against a subsequent cerebral ischemic event when delivered 2 hours before ischemia. Pretreatment with EA reduced infarct volumes, improved neurological outcome, inhibited neuronal apoptosis, and increased the Bcl-2-to-Bax ratio after reperfusion, and the beneficial effects were attenuated by TAT-εV1-2. In addition, the blockade of cannabinoid receptor type 1, but not cannabinoid receptor type 2 receptor, reversed the increase in εPKC activation and neuroprotection induced by EA pretreatment.
EA pretreatment may activate endogenous εPKC-mediated anti-apoptosis to protect against ischemic damage after focal cerebral ischemia via cannabinoid receptor type 1, which represents a new mechanism of EA pretreatment-induced rapid tolerance to focal cerebral ischemia in rats.</description><identifier>ISSN: 0039-2499</identifier><identifier>ISSN: 1524-4628</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.110.597336</identifier><identifier>PMID: 21183751</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Apoptosis - physiology ; Biological and medical sciences ; Brain Ischemia - metabolism ; Brain Ischemia - prevention & control ; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges ; Electroacupuncture - methods ; Enzyme Activation - physiology ; Fundamental and applied biological sciences. Psychology ; Male ; Medical sciences ; Neurology ; Protein Kinase C-epsilon - metabolism ; Protein Kinase C-epsilon - physiology ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1 - physiology ; Time Factors ; Treatment Outcome ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs</subject><ispartof>Stroke (1970), 2011-02, Vol.42 (2), p.389-396</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c465t-3954b0d9c6966df16878c0728c994379d79d4ecc84c1597262006726e3c35c7b3</citedby><cites>FETCH-LOGICAL-c465t-3954b0d9c6966df16878c0728c994379d79d4ecc84c1597262006726e3c35c7b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3685,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23791036$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21183751$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Li, Xuying</creatorcontrib><creatorcontrib>Chen, Yanke</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Yang, Qianzi</creatorcontrib><creatorcontrib>Chen, Shaoyang</creatorcontrib><creatorcontrib>Min, Yuyuan</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Xiong, Lize</creatorcontrib><title>Activation of Epsilon Protein Kinase C-Mediated Anti-Apoptosis Is Involved in Rapid Tolerance Induced by Electroacupuncture Pretreatment Through Cannabinoid Receptor Type 1</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Our previous study has demonstrated that the rapid tolerance to cerebral ischemia by electroacupuncture (EA) pretreatment was possibly mediated through an endocannabinoid system-related mechanism. The purpose of this study was to investigate whether activation of epsilon protein kinase C (εPKC) was involved in EA pretreatment-induced neuroprotection via cannabinoid receptor type 1 in a rat model of transient focal cerebral ischemia.
The activation of εPKC in the ipsilateral brain tissues after EA pretreatment was investigated in the presence or absence of cannabinoid receptor antagonists. At 2 hours after the end of EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 minutes in rats. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the expression of Bcl-2 and Bax were evaluated after reperfusion in the presence or absence of εPKC-selective peptide inhibitor (TAT-εV1-2) or activator (TAT-ψεRACK).
EA pretreatment enhanced εPKC activation. Systemic delivery of TAT-ψεRACK conferred neuroprotection against a subsequent cerebral ischemic event when delivered 2 hours before ischemia. Pretreatment with EA reduced infarct volumes, improved neurological outcome, inhibited neuronal apoptosis, and increased the Bcl-2-to-Bax ratio after reperfusion, and the beneficial effects were attenuated by TAT-εV1-2. In addition, the blockade of cannabinoid receptor type 1, but not cannabinoid receptor type 2 receptor, reversed the increase in εPKC activation and neuroprotection induced by EA pretreatment.
EA pretreatment may activate endogenous εPKC-mediated anti-apoptosis to protect against ischemic damage after focal cerebral ischemia via cannabinoid receptor type 1, which represents a new mechanism of EA pretreatment-induced rapid tolerance to focal cerebral ischemia in rats.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - prevention & control</subject><subject>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</subject><subject>Electroacupuncture - methods</subject><subject>Enzyme Activation - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Protein Kinase C-epsilon - metabolism</subject><subject>Protein Kinase C-epsilon - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Cannabinoid, CB1 - physiology</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0039-2499</issn><issn>1524-4628</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi0EokvhDRDyBXFK8b_Y8TFaLbRqUdESzpHjzFKjrB1sZ6V9Jx4SV7uUI9JI49H85ht5PoTeUnJFqaQfv3Xb-9tNe92WklzVWnEun6EVrZmohGTNc7QihOuKCa0v0KuUfhJCGG_ql-iCUdpwVdMV-t3a7A4mu-Bx2OHNnNxUnl9jyOA8vnXeJMDr6guMzmQYceuzq9o5zDkkl_BNCX8I06G0Cr81sxtxFyaIxlsovXGxpTUc8WYCm2MwdpkXb_MSoWyBHMHkPfiMu4cYlh8PeG28N4PzoQhtwUJZFHF3nAHT1-jFzkwJ3pzzJfr-adOtr6u7-8836_auskLWueK6FgMZtZVaynFHZaMaSxRrrNaCKz2WEGBtIywtd2OSESJLAm55bdXAL9GHk-4cw68FUu73LlmYJuMhLKnXRJVBptR_yUYowZkgupDiRNoYUoqw6-fo9iYee0r6R0P7J0NLSfqToWXs3XnBMuxhfBr662AB3p8Bk6yZdo93d-kfV_5LSRH6A0odqxQ</recordid><startdate>20110201</startdate><enddate>20110201</enddate><creator>Wang, Qiang</creator><creator>Li, Xuying</creator><creator>Chen, Yanke</creator><creator>Wang, Feng</creator><creator>Yang, Qianzi</creator><creator>Chen, Shaoyang</creator><creator>Min, Yuyuan</creator><creator>Li, Xin</creator><creator>Xiong, Lize</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20110201</creationdate><title>Activation of Epsilon Protein Kinase C-Mediated Anti-Apoptosis Is Involved in Rapid Tolerance Induced by Electroacupuncture Pretreatment Through Cannabinoid Receptor Type 1</title><author>Wang, Qiang ; Li, Xuying ; Chen, Yanke ; Wang, Feng ; Yang, Qianzi ; Chen, Shaoyang ; Min, Yuyuan ; Li, Xin ; Xiong, Lize</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c465t-3954b0d9c6966df16878c0728c994379d79d4ecc84c1597262006726e3c35c7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - prevention & control</topic><topic>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</topic><topic>Electroacupuncture - methods</topic><topic>Enzyme Activation - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Protein Kinase C-epsilon - metabolism</topic><topic>Protein Kinase C-epsilon - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Cannabinoid, CB1 - physiology</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Li, Xuying</creatorcontrib><creatorcontrib>Chen, Yanke</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Yang, Qianzi</creatorcontrib><creatorcontrib>Chen, Shaoyang</creatorcontrib><creatorcontrib>Min, Yuyuan</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Xiong, Lize</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Qiang</au><au>Li, Xuying</au><au>Chen, Yanke</au><au>Wang, Feng</au><au>Yang, Qianzi</au><au>Chen, Shaoyang</au><au>Min, Yuyuan</au><au>Li, Xin</au><au>Xiong, Lize</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Epsilon Protein Kinase C-Mediated Anti-Apoptosis Is Involved in Rapid Tolerance Induced by Electroacupuncture Pretreatment Through Cannabinoid Receptor Type 1</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2011-02-01</date><risdate>2011</risdate><volume>42</volume><issue>2</issue><spage>389</spage><epage>396</epage><pages>389-396</pages><issn>0039-2499</issn><issn>1524-4628</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Our previous study has demonstrated that the rapid tolerance to cerebral ischemia by electroacupuncture (EA) pretreatment was possibly mediated through an endocannabinoid system-related mechanism. The purpose of this study was to investigate whether activation of epsilon protein kinase C (εPKC) was involved in EA pretreatment-induced neuroprotection via cannabinoid receptor type 1 in a rat model of transient focal cerebral ischemia.
The activation of εPKC in the ipsilateral brain tissues after EA pretreatment was investigated in the presence or absence of cannabinoid receptor antagonists. At 2 hours after the end of EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 minutes in rats. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the expression of Bcl-2 and Bax were evaluated after reperfusion in the presence or absence of εPKC-selective peptide inhibitor (TAT-εV1-2) or activator (TAT-ψεRACK).
EA pretreatment enhanced εPKC activation. Systemic delivery of TAT-ψεRACK conferred neuroprotection against a subsequent cerebral ischemic event when delivered 2 hours before ischemia. Pretreatment with EA reduced infarct volumes, improved neurological outcome, inhibited neuronal apoptosis, and increased the Bcl-2-to-Bax ratio after reperfusion, and the beneficial effects were attenuated by TAT-εV1-2. In addition, the blockade of cannabinoid receptor type 1, but not cannabinoid receptor type 2 receptor, reversed the increase in εPKC activation and neuroprotection induced by EA pretreatment.
EA pretreatment may activate endogenous εPKC-mediated anti-apoptosis to protect against ischemic damage after focal cerebral ischemia via cannabinoid receptor type 1, which represents a new mechanism of EA pretreatment-induced rapid tolerance to focal cerebral ischemia in rats.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>21183751</pmid><doi>10.1161/STROKEAHA.110.597336</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Apoptosis - physiology Biological and medical sciences Brain Ischemia - metabolism Brain Ischemia - prevention & control Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges Electroacupuncture - methods Enzyme Activation - physiology Fundamental and applied biological sciences. Psychology Male Medical sciences Neurology Protein Kinase C-epsilon - metabolism Protein Kinase C-epsilon - physiology Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB1 - physiology Time Factors Treatment Outcome Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs |
| title | Activation of Epsilon Protein Kinase C-Mediated Anti-Apoptosis Is Involved in Rapid Tolerance Induced by Electroacupuncture Pretreatment Through Cannabinoid Receptor Type 1 |
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