Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons
Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP medi...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-09, Vol.9 (9), p.e105944 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 9 |
| container_start_page | e105944 |
| container_title | PloS one |
| container_volume | 9 |
| creator | Gong, Gu Yuan, Libang Cai, Lin Ran, Maorong Zhang, Yulan Gong, Huaqu Dai, Xuemei Wu, Wei Dong, Hailong |
| description | Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways. |
| doi_str_mv | 10.1371/journal.pone.0105944 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1563701813</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A418138071</galeid><doaj_id>oai_doaj_org_article_3070cbb8e86b477cb3942739c9c89f18</doaj_id><sourcerecordid>A418138071</sourcerecordid><originalsourceid>FETCH-LOGICAL-c692t-a575db548396fde543e18120b9e48704533863cd6cc2e7ac6b3316df86824a7d3</originalsourceid><addsrcrecordid>eNqNk2Fr1DAYx4sobk6_gWhAEHxxt6Rp0_aNcIypxyaTOX0b0vTpNSOXxCSdd34yP565223sQEH6oiXP7_k1_JMny14SPCW0IsfXdvRG6KmzBqaY4LIpikfZIWloPmE5po8ffB9kz0K4xrikNWNPs4O8zGnVYHaY_b6C6MUS4rDWbu3FL2UAhdE5DyFAQKloggITkV2tF2AmCz1KGwB14Ly6EVFZM1GmGyV0SFpjYKUMzRGstoZURcKkCmiNhLMu2qACulECxQHQ6eUZOc63hKM1-jz7coaciMNPsUbKIDnqOPokHpRzVoqlExoZGL014Xn2pBc6wIvd-yj79uH06uTT5Pzi4_xkdj6RrMnjRJRV2bVlUdOG9R2UBQVSkxy3DRR1hYuSpkio7JiUOVRCspZSwrq-ZnVeiKqjR9nrW6_TNvBd6IGTktEKJxVNxPyW6Ky45imVpfBrboXi2wXrF1z4qKQGTnGFZdvWULO2qCrZ0qbIK9rIRtZNT-rker_729guoZMpeC_0nnS_YtTAF_aGF4Q1Jd4I3uwE3v4YIcR_bHlHLUTalTK9TTK5VEHyWbEhalyRRE3_QqWng6VKZw29Sut7De_2GhITYRUXYgyBz79e_j978X2fffuAHUDoOASrx83lC_tgcQtKb0Pw0N8nRzDfTM1dGnwzNXw3Nant1cPU75vuxoT-AT5IFaQ</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1563701813</pqid></control><display><type>article</type><title>Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Gong, Gu ; Yuan, Libang ; Cai, Lin ; Ran, Maorong ; Zhang, Yulan ; Gong, Huaqu ; Dai, Xuemei ; Wu, Wei ; Dong, Hailong</creator><contributor>Gallyas, Ferenc</contributor><creatorcontrib>Gong, Gu ; Yuan, Libang ; Cai, Lin ; Ran, Maorong ; Zhang, Yulan ; Gong, Huaqu ; Dai, Xuemei ; Wu, Wei ; Dong, Hailong ; Gallyas, Ferenc</creatorcontrib><description>Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0105944</identifier><identifier>PMID: 25237906</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal cognition ; Animals ; Apoptosis ; Apoptosis - drug effects ; Bax protein ; Bcl-2 protein ; Biology and Life Sciences ; Cells, Cultured ; Communication ; Connexin 32 ; Connexins - genetics ; Connexins - metabolism ; Cytometry ; Deprivation ; Experiments ; Extracellular signal-regulated kinase ; Fibroblasts ; Flow cytometry ; Gap Junction beta-1 Protein ; Gene Expression Regulation - drug effects ; Gene Knockdown Techniques ; Glucose ; Glucose - metabolism ; Growth factors ; Herbal medicine ; Hippocampus ; Hippocampus - cytology ; Hippocampus - drug effects ; Hospitals ; Injuries ; Ischemia ; Laboratory animals ; MAP kinase ; MAP Kinase Signaling System - drug effects ; Medical treatment ; Medicine and Health Sciences ; Neurons ; Neurons - drug effects ; Oxygen ; Oxygen - metabolism ; Phosphorylation ; Pyrazines - pharmacology ; Rats, Wistar ; RNA Interference ; Rodents ; siRNA ; Stem cells ; Stroke ; Traumatic brain injury ; Viability</subject><ispartof>PloS one, 2014-09, Vol.9 (9), p.e105944</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Gong et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Gong et al 2014 Gong et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-a575db548396fde543e18120b9e48704533863cd6cc2e7ac6b3316df86824a7d3</citedby><cites>FETCH-LOGICAL-c692t-a575db548396fde543e18120b9e48704533863cd6cc2e7ac6b3316df86824a7d3</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/PMC4169508/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169508/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25237906$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gallyas, Ferenc</contributor><creatorcontrib>Gong, Gu</creatorcontrib><creatorcontrib>Yuan, Libang</creatorcontrib><creatorcontrib>Cai, Lin</creatorcontrib><creatorcontrib>Ran, Maorong</creatorcontrib><creatorcontrib>Zhang, Yulan</creatorcontrib><creatorcontrib>Gong, Huaqu</creatorcontrib><creatorcontrib>Dai, Xuemei</creatorcontrib><creatorcontrib>Wu, Wei</creatorcontrib><creatorcontrib>Dong, Hailong</creatorcontrib><title>Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways.</description><subject>Animal cognition</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Biology and Life Sciences</subject><subject>Cells, Cultured</subject><subject>Communication</subject><subject>Connexin 32</subject><subject>Connexins - genetics</subject><subject>Connexins - metabolism</subject><subject>Cytometry</subject><subject>Deprivation</subject><subject>Experiments</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fibroblasts</subject><subject>Flow cytometry</subject><subject>Gap Junction beta-1 Protein</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Knockdown Techniques</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Growth factors</subject><subject>Herbal medicine</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - drug effects</subject><subject>Hospitals</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Medical treatment</subject><subject>Medicine and Health Sciences</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Phosphorylation</subject><subject>Pyrazines - pharmacology</subject><subject>Rats, Wistar</subject><subject>RNA Interference</subject><subject>Rodents</subject><subject>siRNA</subject><subject>Stem cells</subject><subject>Stroke</subject><subject>Traumatic brain injury</subject><subject>Viability</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk2Fr1DAYx4sobk6_gWhAEHxxt6Rp0_aNcIypxyaTOX0b0vTpNSOXxCSdd34yP565223sQEH6oiXP7_k1_JMny14SPCW0IsfXdvRG6KmzBqaY4LIpikfZIWloPmE5po8ffB9kz0K4xrikNWNPs4O8zGnVYHaY_b6C6MUS4rDWbu3FL2UAhdE5DyFAQKloggITkV2tF2AmCz1KGwB14Ly6EVFZM1GmGyV0SFpjYKUMzRGstoZURcKkCmiNhLMu2qACulECxQHQ6eUZOc63hKM1-jz7coaciMNPsUbKIDnqOPokHpRzVoqlExoZGL014Xn2pBc6wIvd-yj79uH06uTT5Pzi4_xkdj6RrMnjRJRV2bVlUdOG9R2UBQVSkxy3DRR1hYuSpkio7JiUOVRCspZSwrq-ZnVeiKqjR9nrW6_TNvBd6IGTktEKJxVNxPyW6Ky45imVpfBrboXi2wXrF1z4qKQGTnGFZdvWULO2qCrZ0qbIK9rIRtZNT-rker_729guoZMpeC_0nnS_YtTAF_aGF4Q1Jd4I3uwE3v4YIcR_bHlHLUTalTK9TTK5VEHyWbEhalyRRE3_QqWng6VKZw29Sut7De_2GhITYRUXYgyBz79e_j978X2fffuAHUDoOASrx83lC_tgcQtKb0Pw0N8nRzDfTM1dGnwzNXw3Nant1cPU75vuxoT-AT5IFaQ</recordid><startdate>20140919</startdate><enddate>20140919</enddate><creator>Gong, Gu</creator><creator>Yuan, Libang</creator><creator>Cai, Lin</creator><creator>Ran, Maorong</creator><creator>Zhang, Yulan</creator><creator>Gong, Huaqu</creator><creator>Dai, Xuemei</creator><creator>Wu, Wei</creator><creator>Dong, Hailong</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140919</creationdate><title>Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons</title><author>Gong, Gu ; Yuan, Libang ; Cai, Lin ; Ran, Maorong ; Zhang, Yulan ; Gong, Huaqu ; Dai, Xuemei ; Wu, Wei ; Dong, Hailong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-a575db548396fde543e18120b9e48704533863cd6cc2e7ac6b3316df86824a7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animal cognition</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Biology and Life Sciences</topic><topic>Cells, Cultured</topic><topic>Communication</topic><topic>Connexin 32</topic><topic>Connexins - genetics</topic><topic>Connexins - metabolism</topic><topic>Cytometry</topic><topic>Deprivation</topic><topic>Experiments</topic><topic>Extracellular signal-regulated kinase</topic><topic>Fibroblasts</topic><topic>Flow cytometry</topic><topic>Gap Junction beta-1 Protein</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Knockdown Techniques</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Growth factors</topic><topic>Herbal medicine</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - drug effects</topic><topic>Hospitals</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Laboratory animals</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Medical treatment</topic><topic>Medicine and Health Sciences</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Oxygen</topic><topic>Oxygen - metabolism</topic><topic>Phosphorylation</topic><topic>Pyrazines - pharmacology</topic><topic>Rats, Wistar</topic><topic>RNA Interference</topic><topic>Rodents</topic><topic>siRNA</topic><topic>Stem cells</topic><topic>Stroke</topic><topic>Traumatic brain injury</topic><topic>Viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gong, Gu</creatorcontrib><creatorcontrib>Yuan, Libang</creatorcontrib><creatorcontrib>Cai, Lin</creatorcontrib><creatorcontrib>Ran, Maorong</creatorcontrib><creatorcontrib>Zhang, Yulan</creatorcontrib><creatorcontrib>Gong, Huaqu</creatorcontrib><creatorcontrib>Dai, Xuemei</creatorcontrib><creatorcontrib>Wu, Wei</creatorcontrib><creatorcontrib>Dong, Hailong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gong, Gu</au><au>Yuan, Libang</au><au>Cai, Lin</au><au>Ran, Maorong</au><au>Zhang, Yulan</au><au>Gong, Huaqu</au><au>Dai, Xuemei</au><au>Wu, Wei</au><au>Dong, Hailong</au><au>Gallyas, Ferenc</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-09-19</date><risdate>2014</risdate><volume>9</volume><issue>9</issue><spage>e105944</spage><pages>e105944-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25237906</pmid><doi>10.1371/journal.pone.0105944</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-09, Vol.9 (9), p.e105944 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1563701813 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animal cognition Animals Apoptosis Apoptosis - drug effects Bax protein Bcl-2 protein Biology and Life Sciences Cells, Cultured Communication Connexin 32 Connexins - genetics Connexins - metabolism Cytometry Deprivation Experiments Extracellular signal-regulated kinase Fibroblasts Flow cytometry Gap Junction beta-1 Protein Gene Expression Regulation - drug effects Gene Knockdown Techniques Glucose Glucose - metabolism Growth factors Herbal medicine Hippocampus Hippocampus - cytology Hippocampus - drug effects Hospitals Injuries Ischemia Laboratory animals MAP kinase MAP Kinase Signaling System - drug effects Medical treatment Medicine and Health Sciences Neurons Neurons - drug effects Oxygen Oxygen - metabolism Phosphorylation Pyrazines - pharmacology Rats, Wistar RNA Interference Rodents siRNA Stem cells Stroke Traumatic brain injury Viability |
| title | Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T06%3A14%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tetramethylpyrazine%20suppresses%20transient%20oxygen-glucose%20deprivation-induced%20connexin32%20expression%20and%20cell%20apoptosis%20via%20the%20ERK1/2%20and%20p38%20MAPK%20pathway%20in%20cultured%20hippocampal%20neurons&rft.jtitle=PloS%20one&rft.au=Gong,%20Gu&rft.date=2014-09-19&rft.volume=9&rft.issue=9&rft.spage=e105944&rft.pages=e105944-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0105944&rft_dat=%3Cgale_plos_%3EA418138071%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1563701813&rft_id=info:pmid/25237906&rft_galeid=A418138071&rft_doaj_id=oai_doaj_org_article_3070cbb8e86b477cb3942739c9c89f18&rfr_iscdi=true |