2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice
In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the ef...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2012-04, Vol.13 (4), p.4968-4981 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 4981 |
|---|---|
| container_issue | 4 |
| container_start_page | 4968 |
| container_title | International journal of molecular sciences |
| container_volume | 13 |
| creator | Tanaka, Yoshitaka Fukumitsu, Hidefumi Soumiya, Hitomi Yoshimura, Shinichi Iwama, Toru Furukawa, Shoei |
| description | In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction. |
| doi_str_mv | 10.3390/ijms13044968 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3344259</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1015095831</sourcerecordid><originalsourceid>FETCH-LOGICAL-c445t-61ef8a3199cde6e27faa17ccee00bf443ff9bbdc92baca5b1f88fcc7399ec0cd3</originalsourceid><addsrcrecordid>eNqFkk9v1DAQxSMEoqVw44wsceGwAf9LNr4goYoCUiUucLacyXjXi2MvtlNpPw1fFW9bqoULJ489Pz3NPL-mecnoWyEUfed2c2aCSqn64VFzziTnLaX9-vFJfdY8y3lHKRe8U0-bM8572tfbefOLtxMChuiAGHATwbI9eIK5YFoRQyDO-7iEiZStKQS9A1cyCbikWFLcb11ovfuBxIWSDKD3izeJZLcJxucVsVXTu2KKCxtilwDFxdohCSHeYDoQm-JMABOOqT67YE26ZWpJZgf4vHliqxK-uD8vmu9XH79dfm6vv376cvnhugUpu9L2DO1gBFMKJuyRr60xbA2ASOlopRTWqnGcQPHRgOlGZofBAqyFUggUJnHRvL_T3S_jjFN1pO7j9T652aSDjsbpvzvBbfUm3mghpKymVoE39wIp_lyqf3p2-WiICRiXrBkfOqoYp-L_KGUV7QbBKvr6H3QXl3T0VrOufiJjPesrtbqjIMWcE9qHuRnVx5Do05BU_NXprg_wn1SI3775vfQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1526011616</pqid></control><display><type>article</type><title>2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Tanaka, Yoshitaka ; Fukumitsu, Hidefumi ; Soumiya, Hitomi ; Yoshimura, Shinichi ; Iwama, Toru ; Furukawa, Shoei</creator><creatorcontrib>Tanaka, Yoshitaka ; Fukumitsu, Hidefumi ; Soumiya, Hitomi ; Yoshimura, Shinichi ; Iwama, Toru ; Furukawa, Shoei</creatorcontrib><description>In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms13044968</identifier><identifier>PMID: 22606023</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alzheimer's disease ; Animal models ; Animals ; Blood-Brain Barrier - drug effects ; Body weight ; Brain ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - metabolism ; Cell survival ; Cerebral blood flow ; Cerebral Cortex - cytology ; Cerebral Cortex - pathology ; Cerebral infarction ; Cerebral Infarction - drug therapy ; Chi-square test ; Cortex ; Disease Models, Animal ; Esters ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fatty acids ; Fatty Acids, Monounsaturated - chemistry ; Fatty Acids, Monounsaturated - therapeutic use ; Infarction, Middle Cerebral Artery - drug therapy ; Ischemia ; Kinases ; Male ; Medical prognosis ; Mice ; Mortality ; Nerve Growth Factors - metabolism ; Neurological diseases ; Neurological disorders ; Neuroprotective Agents - chemistry ; Neuroprotective Agents - therapeutic use ; Oxidative Stress - drug effects ; Paralysis ; Paralysis - prevention & control ; Phosphorylation ; Recovery of function ; Stroke ; Veins & arteries</subject><ispartof>International journal of molecular sciences, 2012-04, Vol.13 (4), p.4968-4981</ispartof><rights>Copyright MDPI AG 2012</rights><rights>2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-61ef8a3199cde6e27faa17ccee00bf443ff9bbdc92baca5b1f88fcc7399ec0cd3</citedby><cites>FETCH-LOGICAL-c445t-61ef8a3199cde6e27faa17ccee00bf443ff9bbdc92baca5b1f88fcc7399ec0cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344259/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344259/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22606023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tanaka, Yoshitaka</creatorcontrib><creatorcontrib>Fukumitsu, Hidefumi</creatorcontrib><creatorcontrib>Soumiya, Hitomi</creatorcontrib><creatorcontrib>Yoshimura, Shinichi</creatorcontrib><creatorcontrib>Iwama, Toru</creatorcontrib><creatorcontrib>Furukawa, Shoei</creatorcontrib><title>2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction.</description><subject>Alzheimer's disease</subject><subject>Animal models</subject><subject>Animals</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Body weight</subject><subject>Brain</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Cell survival</subject><subject>Cerebral blood flow</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral infarction</subject><subject>Cerebral Infarction - drug therapy</subject><subject>Chi-square test</subject><subject>Cortex</subject><subject>Disease Models, Animal</subject><subject>Esters</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Fatty acids</subject><subject>Fatty Acids, Monounsaturated - chemistry</subject><subject>Fatty Acids, Monounsaturated - therapeutic use</subject><subject>Infarction, Middle Cerebral Artery - drug therapy</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Mortality</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neurological diseases</subject><subject>Neurological disorders</subject><subject>Neuroprotective Agents - chemistry</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Oxidative Stress - drug effects</subject><subject>Paralysis</subject><subject>Paralysis - prevention & control</subject><subject>Phosphorylation</subject><subject>Recovery of function</subject><subject>Stroke</subject><subject>Veins & arteries</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk9v1DAQxSMEoqVw44wsceGwAf9LNr4goYoCUiUucLacyXjXi2MvtlNpPw1fFW9bqoULJ489Pz3NPL-mecnoWyEUfed2c2aCSqn64VFzziTnLaX9-vFJfdY8y3lHKRe8U0-bM8572tfbefOLtxMChuiAGHATwbI9eIK5YFoRQyDO-7iEiZStKQS9A1cyCbikWFLcb11ovfuBxIWSDKD3izeJZLcJxucVsVXTu2KKCxtilwDFxdohCSHeYDoQm-JMABOOqT67YE26ZWpJZgf4vHliqxK-uD8vmu9XH79dfm6vv376cvnhugUpu9L2DO1gBFMKJuyRr60xbA2ASOlopRTWqnGcQPHRgOlGZofBAqyFUggUJnHRvL_T3S_jjFN1pO7j9T652aSDjsbpvzvBbfUm3mghpKymVoE39wIp_lyqf3p2-WiICRiXrBkfOqoYp-L_KGUV7QbBKvr6H3QXl3T0VrOufiJjPesrtbqjIMWcE9qHuRnVx5Do05BU_NXprg_wn1SI3775vfQ</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>Tanaka, Yoshitaka</creator><creator>Fukumitsu, Hidefumi</creator><creator>Soumiya, Hitomi</creator><creator>Yoshimura, Shinichi</creator><creator>Iwama, Toru</creator><creator>Furukawa, Shoei</creator><general>MDPI AG</general><general>Molecular Diversity Preservation International (MDPI)</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20120401</creationdate><title>2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice</title><author>Tanaka, Yoshitaka ; Fukumitsu, Hidefumi ; Soumiya, Hitomi ; Yoshimura, Shinichi ; Iwama, Toru ; Furukawa, Shoei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-61ef8a3199cde6e27faa17ccee00bf443ff9bbdc92baca5b1f88fcc7399ec0cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Alzheimer's disease</topic><topic>Animal models</topic><topic>Animals</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Body weight</topic><topic>Brain</topic><topic>Brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Cell survival</topic><topic>Cerebral blood flow</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral infarction</topic><topic>Cerebral Infarction - drug therapy</topic><topic>Chi-square test</topic><topic>Cortex</topic><topic>Disease Models, Animal</topic><topic>Esters</topic><topic>Extracellular signal-regulated kinase</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Fatty acids</topic><topic>Fatty Acids, Monounsaturated - chemistry</topic><topic>Fatty Acids, Monounsaturated - therapeutic use</topic><topic>Infarction, Middle Cerebral Artery - drug therapy</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>Mortality</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neurological diseases</topic><topic>Neurological disorders</topic><topic>Neuroprotective Agents - chemistry</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Oxidative Stress - drug effects</topic><topic>Paralysis</topic><topic>Paralysis - prevention & control</topic><topic>Phosphorylation</topic><topic>Recovery of function</topic><topic>Stroke</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanaka, Yoshitaka</creatorcontrib><creatorcontrib>Fukumitsu, Hidefumi</creatorcontrib><creatorcontrib>Soumiya, Hitomi</creatorcontrib><creatorcontrib>Yoshimura, Shinichi</creatorcontrib><creatorcontrib>Iwama, Toru</creatorcontrib><creatorcontrib>Furukawa, Shoei</creatorcontrib><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>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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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 Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanaka, Yoshitaka</au><au>Fukumitsu, Hidefumi</au><au>Soumiya, Hitomi</au><au>Yoshimura, Shinichi</au><au>Iwama, Toru</au><au>Furukawa, Shoei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>13</volume><issue>4</issue><spage>4968</spage><epage>4981</epage><pages>4968-4981</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>22606023</pmid><doi>10.3390/ijms13044968</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2012-04, Vol.13 (4), p.4968-4981 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3344259 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Alzheimer's disease Animal models Animals Blood-Brain Barrier - drug effects Body weight Brain Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Cell survival Cerebral blood flow Cerebral Cortex - cytology Cerebral Cortex - pathology Cerebral infarction Cerebral Infarction - drug therapy Chi-square test Cortex Disease Models, Animal Esters Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - metabolism Fatty acids Fatty Acids, Monounsaturated - chemistry Fatty Acids, Monounsaturated - therapeutic use Infarction, Middle Cerebral Artery - drug therapy Ischemia Kinases Male Medical prognosis Mice Mortality Nerve Growth Factors - metabolism Neurological diseases Neurological disorders Neuroprotective Agents - chemistry Neuroprotective Agents - therapeutic use Oxidative Stress - drug effects Paralysis Paralysis - prevention & control Phosphorylation Recovery of function Stroke Veins & arteries |
| title | 2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T03%3A25%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=2-decenoic%20acid%20ethyl%20ester,%20a%20compound%20that%20elicits%20neurotrophin-like%20intracellular%20signals,%20facilitating%20functional%20recovery%20from%20cerebral%20infarction%20in%20mice&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Tanaka,%20Yoshitaka&rft.date=2012-04-01&rft.volume=13&rft.issue=4&rft.spage=4968&rft.epage=4981&rft.pages=4968-4981&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms13044968&rft_dat=%3Cproquest_pubme%3E1015095831%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1526011616&rft_id=info:pmid/22606023&rfr_iscdi=true |