Pretreated duloxetine protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury through decreases of glial activation and oxidative stress
Abstract Duloxetine (DXT), a serotonin/norepinephrine reuptake inhibitor, is widely used for the treatment of major depressive disorders. In the present study, we investigated the neuroprotective effect of pre-treated DXT in the hippocampal CA1 region following transient global cerebral ischemia. Pr...
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| Veröffentlicht in: | Journal of the neurological sciences 2016-11, Vol.370, p.229-236 |
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| container_title | Journal of the neurological sciences |
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| creator | Lee, Tae-Kyeong Park, Joon Ha Ahn, Ji Hyeon Shin, Myoung Cheol Cho, Jun Hwi Bae, Eun Joo Kim, Young-Myeong Won, Moo-Ho Lee, Choong-Hyun |
| description | Abstract Duloxetine (DXT), a serotonin/norepinephrine reuptake inhibitor, is widely used for the treatment of major depressive disorders. In the present study, we investigated the neuroprotective effect of pre-treated DXT in the hippocampal CA1 region following transient global cerebral ischemia. Pre-treatment with 40 mg/kg DXT protected pyramidal neurons in the CA1 region from ischemia-reperfusion injury. In addition, pre-treatment with DXT reduced ischemia-induced activations of microglia and astrocytes in the ischemic CA1 region. On the other hand, we found that pre-treatment with DXT did not increase 4-hydroxy-2-noneal (a marker for lipid peroxidation) and significantly increased the expression of Cu, Zn-superoxide dismutase, an antioxidant, in the CA1 pyramidal neurons compared with non-treated those after ischemia-reperfusion. These results indicate that pre-treated DXT has neuroprotective effect against transient global cerebral ischemia and suggest that the neuroprotective effect of DXT may be due to the attenuation of ischemia-induced glial activation as well as the decrease of oxidative stress. |
| doi_str_mv | 10.1016/j.jns.2016.09.059 |
| format | Article |
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In the present study, we investigated the neuroprotective effect of pre-treated DXT in the hippocampal CA1 region following transient global cerebral ischemia. Pre-treatment with 40 mg/kg DXT protected pyramidal neurons in the CA1 region from ischemia-reperfusion injury. In addition, pre-treatment with DXT reduced ischemia-induced activations of microglia and astrocytes in the ischemic CA1 region. On the other hand, we found that pre-treatment with DXT did not increase 4-hydroxy-2-noneal (a marker for lipid peroxidation) and significantly increased the expression of Cu, Zn-superoxide dismutase, an antioxidant, in the CA1 pyramidal neurons compared with non-treated those after ischemia-reperfusion. These results indicate that pre-treated DXT has neuroprotective effect against transient global cerebral ischemia and suggest that the neuroprotective effect of DXT may be due to the attenuation of ischemia-induced glial activation as well as the decrease of oxidative stress.</description><identifier>ISSN: 0022-510X</identifier><identifier>EISSN: 1878-5883</identifier><identifier>DOI: 10.1016/j.jns.2016.09.059</identifier><identifier>PMID: 27772765</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Brain Ischemia - drug therapy ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; CA1 Region, Hippocampal - drug effects ; CA1 Region, Hippocampal - metabolism ; CA1 Region, Hippocampal - pathology ; Delayed neuronal death ; Drug Evaluation, Preclinical ; Duloxetine ; Duloxetine Hydrochloride - pharmacology ; Gerbillinae ; Glial activation ; Male ; Neuroglia - drug effects ; Neuroglia - metabolism ; Neuroglia - pathology ; Neurology ; Neuroprotective Agents - pharmacology ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Pyramidal Cells - drug effects ; Pyramidal Cells - metabolism ; Pyramidal Cells - pathology ; Pyramidal neurons ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Serotonin and Noradrenaline Reuptake Inhibitors - pharmacology ; Superoxide Dismutase-1 - metabolism ; Transient global cerebral ischemia</subject><ispartof>Journal of the neurological sciences, 2016-11, Vol.370, p.229-236</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-7e8bbfcd480f4c6bee5ba154541c04fde9f6099606f928aadc3769cb7c81fdfe3</citedby><cites>FETCH-LOGICAL-c474t-7e8bbfcd480f4c6bee5ba154541c04fde9f6099606f928aadc3769cb7c81fdfe3</cites><orcidid>0000-0002-7178-6501</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jns.2016.09.059$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27772765$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Tae-Kyeong</creatorcontrib><creatorcontrib>Park, Joon Ha</creatorcontrib><creatorcontrib>Ahn, Ji Hyeon</creatorcontrib><creatorcontrib>Shin, Myoung Cheol</creatorcontrib><creatorcontrib>Cho, Jun Hwi</creatorcontrib><creatorcontrib>Bae, Eun Joo</creatorcontrib><creatorcontrib>Kim, Young-Myeong</creatorcontrib><creatorcontrib>Won, Moo-Ho</creatorcontrib><creatorcontrib>Lee, Choong-Hyun</creatorcontrib><title>Pretreated duloxetine protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury through decreases of glial activation and oxidative stress</title><title>Journal of the neurological sciences</title><addtitle>J Neurol Sci</addtitle><description>Abstract Duloxetine (DXT), a serotonin/norepinephrine reuptake inhibitor, is widely used for the treatment of major depressive disorders. In the present study, we investigated the neuroprotective effect of pre-treated DXT in the hippocampal CA1 region following transient global cerebral ischemia. Pre-treatment with 40 mg/kg DXT protected pyramidal neurons in the CA1 region from ischemia-reperfusion injury. In addition, pre-treatment with DXT reduced ischemia-induced activations of microglia and astrocytes in the ischemic CA1 region. On the other hand, we found that pre-treatment with DXT did not increase 4-hydroxy-2-noneal (a marker for lipid peroxidation) and significantly increased the expression of Cu, Zn-superoxide dismutase, an antioxidant, in the CA1 pyramidal neurons compared with non-treated those after ischemia-reperfusion. These results indicate that pre-treated DXT has neuroprotective effect against transient global cerebral ischemia and suggest that the neuroprotective effect of DXT may be due to the attenuation of ischemia-induced glial activation as well as the decrease of oxidative stress.</description><subject>Animals</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>CA1 Region, Hippocampal - drug effects</subject><subject>CA1 Region, Hippocampal - metabolism</subject><subject>CA1 Region, Hippocampal - pathology</subject><subject>Delayed neuronal death</subject><subject>Drug Evaluation, Preclinical</subject><subject>Duloxetine</subject><subject>Duloxetine Hydrochloride - pharmacology</subject><subject>Gerbillinae</subject><subject>Glial activation</subject><subject>Male</subject><subject>Neuroglia - drug effects</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>Neurology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - metabolism</subject><subject>Pyramidal Cells - pathology</subject><subject>Pyramidal neurons</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Serotonin and Noradrenaline Reuptake Inhibitors - pharmacology</subject><subject>Superoxide Dismutase-1 - metabolism</subject><subject>Transient global cerebral ischemia</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ksuKFDEUhoMoTjv6AG4kSzdVJnVJJQjC0HiDAQUV3IVUcjKdsiopk9Qw_S4-rGl6dOHCVS78_39y8h2EnlNSU0LZq6mefKqbsq2JqEkvHqAd5QOves7bh2hHSNNUPSXfL9CTlCZCCONcPEYXzTAMzcD6Hfr1OUKOoDIYbLY53EF2HvAaQwadEz64dQ1aLaua8f6K4vUY1eJMOXnYYvAJ2xgW7JI-wOJUFWGFaLfkgsfOT1s84nyIYbs5YAO6FEqQcLD4ZnYlQ-nsblU-iZU3ONyV5HIDOJU3pfQUPbJqTvDsfr1E3969_br_UF1_ev9xf3Vd6W7ocjUAH0erTceJ7TQbAfpR0b7rO6pJZw0Iy4gQjDArGq6U0e3AhB4Hzak1FtpL9PKcW9r-uUHKcikNwTwrD2FLkvK276loBStSepbqGFKKYOUa3aLiUVIiT1DkJAsUeYIiiZAFSvG8uI_fxgXMX8cfCkXw-iyA0uStgyiTduA1GBcLBWmC-2_8m3_cenbeaTX_gCOkKWzRl9-TVKZGEvnlNBWnoaCsJazpuvY3aEO4GQ</recordid><startdate>20161115</startdate><enddate>20161115</enddate><creator>Lee, Tae-Kyeong</creator><creator>Park, Joon Ha</creator><creator>Ahn, Ji Hyeon</creator><creator>Shin, Myoung Cheol</creator><creator>Cho, Jun Hwi</creator><creator>Bae, Eun Joo</creator><creator>Kim, Young-Myeong</creator><creator>Won, Moo-Ho</creator><creator>Lee, Choong-Hyun</creator><general>Elsevier B.V</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>7X8</scope><orcidid>https://orcid.org/0000-0002-7178-6501</orcidid></search><sort><creationdate>20161115</creationdate><title>Pretreated duloxetine protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury through decreases of glial activation and oxidative stress</title><author>Lee, Tae-Kyeong ; Park, Joon Ha ; Ahn, Ji Hyeon ; Shin, Myoung Cheol ; Cho, Jun Hwi ; Bae, Eun Joo ; Kim, Young-Myeong ; Won, Moo-Ho ; Lee, Choong-Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-7e8bbfcd480f4c6bee5ba154541c04fde9f6099606f928aadc3769cb7c81fdfe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>CA1 Region, Hippocampal - drug effects</topic><topic>CA1 Region, Hippocampal - metabolism</topic><topic>CA1 Region, Hippocampal - pathology</topic><topic>Delayed neuronal death</topic><topic>Drug Evaluation, Preclinical</topic><topic>Duloxetine</topic><topic>Duloxetine Hydrochloride - pharmacology</topic><topic>Gerbillinae</topic><topic>Glial activation</topic><topic>Male</topic><topic>Neuroglia - drug effects</topic><topic>Neuroglia - metabolism</topic><topic>Neuroglia - pathology</topic><topic>Neurology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - metabolism</topic><topic>Pyramidal Cells - pathology</topic><topic>Pyramidal neurons</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Serotonin and Noradrenaline Reuptake Inhibitors - pharmacology</topic><topic>Superoxide Dismutase-1 - metabolism</topic><topic>Transient global cerebral ischemia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Tae-Kyeong</creatorcontrib><creatorcontrib>Park, Joon Ha</creatorcontrib><creatorcontrib>Ahn, Ji Hyeon</creatorcontrib><creatorcontrib>Shin, Myoung Cheol</creatorcontrib><creatorcontrib>Cho, Jun Hwi</creatorcontrib><creatorcontrib>Bae, Eun Joo</creatorcontrib><creatorcontrib>Kim, Young-Myeong</creatorcontrib><creatorcontrib>Won, Moo-Ho</creatorcontrib><creatorcontrib>Lee, Choong-Hyun</creatorcontrib><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><jtitle>Journal of the neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Tae-Kyeong</au><au>Park, Joon Ha</au><au>Ahn, Ji Hyeon</au><au>Shin, Myoung Cheol</au><au>Cho, Jun Hwi</au><au>Bae, Eun Joo</au><au>Kim, Young-Myeong</au><au>Won, Moo-Ho</au><au>Lee, Choong-Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pretreated duloxetine protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury through decreases of glial activation and oxidative stress</atitle><jtitle>Journal of the neurological sciences</jtitle><addtitle>J Neurol Sci</addtitle><date>2016-11-15</date><risdate>2016</risdate><volume>370</volume><spage>229</spage><epage>236</epage><pages>229-236</pages><issn>0022-510X</issn><eissn>1878-5883</eissn><abstract>Abstract Duloxetine (DXT), a serotonin/norepinephrine reuptake inhibitor, is widely used for the treatment of major depressive disorders. In the present study, we investigated the neuroprotective effect of pre-treated DXT in the hippocampal CA1 region following transient global cerebral ischemia. Pre-treatment with 40 mg/kg DXT protected pyramidal neurons in the CA1 region from ischemia-reperfusion injury. In addition, pre-treatment with DXT reduced ischemia-induced activations of microglia and astrocytes in the ischemic CA1 region. On the other hand, we found that pre-treatment with DXT did not increase 4-hydroxy-2-noneal (a marker for lipid peroxidation) and significantly increased the expression of Cu, Zn-superoxide dismutase, an antioxidant, in the CA1 pyramidal neurons compared with non-treated those after ischemia-reperfusion. These results indicate that pre-treated DXT has neuroprotective effect against transient global cerebral ischemia and suggest that the neuroprotective effect of DXT may be due to the attenuation of ischemia-induced glial activation as well as the decrease of oxidative stress.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27772765</pmid><doi>10.1016/j.jns.2016.09.059</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-7178-6501</orcidid></addata></record> |
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| subjects | Animals Brain Ischemia - drug therapy Brain Ischemia - metabolism Brain Ischemia - pathology CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - metabolism CA1 Region, Hippocampal - pathology Delayed neuronal death Drug Evaluation, Preclinical Duloxetine Duloxetine Hydrochloride - pharmacology Gerbillinae Glial activation Male Neuroglia - drug effects Neuroglia - metabolism Neuroglia - pathology Neurology Neuroprotective Agents - pharmacology Oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Pyramidal Cells - drug effects Pyramidal Cells - metabolism Pyramidal Cells - pathology Pyramidal neurons Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Serotonin and Noradrenaline Reuptake Inhibitors - pharmacology Superoxide Dismutase-1 - metabolism Transient global cerebral ischemia |
| title | Pretreated duloxetine protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury through decreases of glial activation and oxidative stress |
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