Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model
We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were e...
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| Veröffentlicht in: | International journal of immunopathology and pharmacology 2017-06, Vol.30 (2), p.123-129 |
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| description | We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). In addition, rat primary neuronal cells were isolated and cultured in oxygen-glucose deprivation (OGD) conditions. After pretreatment with TSN, cell viability and apoptosis were observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. The expressions of Bax and B-cell lymphoma 2 (Bcl-2) were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. Compared with untreated cerebral infarction rat, TSN treatment significantly reduced cerebral infarct volume, cerebral edema, and neurological deficits score (P < 0.05). Cell apoptosis as well as the levels of IL-6, TNF-α, and CRP in hippocampus and cortex of cerebral infarction rat were inhibited after pretreatment with TSN (P < 0.05). Furthermore, TSN remarkably increased cell viability and inhibited cell apoptosis ratio (P < 0.05) in OGD-induced rat neuronal cells. Besides, TSN significantly downregulated the expression of Bax and upregulated Bcl-2 (P < 0.05). TSN IIA has a preventive effect on cerebral infarction by inhibiting neuronal cell apoptosis and inflammatory response in vitro and in vivo. |
| doi_str_mv | 10.1177/0394632017703274 |
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The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). In addition, rat primary neuronal cells were isolated and cultured in oxygen-glucose deprivation (OGD) conditions. After pretreatment with TSN, cell viability and apoptosis were observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. The expressions of Bax and B-cell lymphoma 2 (Bcl-2) were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. Compared with untreated cerebral infarction rat, TSN treatment significantly reduced cerebral infarct volume, cerebral edema, and neurological deficits score (P < 0.05). Cell apoptosis as well as the levels of IL-6, TNF-α, and CRP in hippocampus and cortex of cerebral infarction rat were inhibited after pretreatment with TSN (P < 0.05). Furthermore, TSN remarkably increased cell viability and inhibited cell apoptosis ratio (P < 0.05) in OGD-induced rat neuronal cells. Besides, TSN significantly downregulated the expression of Bax and upregulated Bcl-2 (P < 0.05). TSN IIA has a preventive effect on cerebral infarction by inhibiting neuronal cell apoptosis and inflammatory response in vitro and in vivo.</description><identifier>ISSN: 2058-7384</identifier><identifier>ISSN: 0394-6320</identifier><identifier>EISSN: 2058-7384</identifier><identifier>DOI: 10.1177/0394632017703274</identifier><identifier>PMID: 28402151</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Abietanes - pharmacology ; Abietanes - therapeutic use ; Animals ; Apoptosis ; Apoptosis - drug effects ; Bax protein ; Bcl-2 protein ; Brain - drug effects ; Brain - metabolism ; Brain - pathology ; C-reactive protein ; C-Reactive Protein - metabolism ; Cell Survival - drug effects ; Cell viability ; Cerebral blood flow ; Cerebral infarction ; Cerebral Infarction - drug therapy ; Cerebral Infarction - metabolism ; Cerebral Infarction - pathology ; DNA nucleotidylexotransferase ; Edema ; Enzyme-linked immunosorbent assay ; Flow cytometry ; Glucose ; Hippocampus ; Inflammation ; Interleukin 6 ; Interleukin-6 - metabolism ; Ischemia ; Lymphocytes B ; Male ; Neurological diseases ; Neurons - drug effects ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Original s ; Oxygen ; Polymerase chain reaction ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats, Sprague-Dawley ; Reverse transcription ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Western blotting</subject><ispartof>International journal of immunopathology and pharmacology, 2017-06, Vol.30 (2), p.123-129</ispartof><rights>The Author(s) 2017</rights><rights>The Author(s) 2017. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2017 2017 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806795/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806795/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,21965,27852,27923,27924,44944,45332,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28402151$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Liang</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Sun, Qiangsan</creatorcontrib><title>Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model</title><title>International journal of immunopathology and pharmacology</title><addtitle>Int J Immunopathol Pharmacol</addtitle><description>We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). In addition, rat primary neuronal cells were isolated and cultured in oxygen-glucose deprivation (OGD) conditions. After pretreatment with TSN, cell viability and apoptosis were observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. The expressions of Bax and B-cell lymphoma 2 (Bcl-2) were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. Compared with untreated cerebral infarction rat, TSN treatment significantly reduced cerebral infarct volume, cerebral edema, and neurological deficits score (P < 0.05). Cell apoptosis as well as the levels of IL-6, TNF-α, and CRP in hippocampus and cortex of cerebral infarction rat were inhibited after pretreatment with TSN (P < 0.05). Furthermore, TSN remarkably increased cell viability and inhibited cell apoptosis ratio (P < 0.05) in OGD-induced rat neuronal cells. Besides, TSN significantly downregulated the expression of Bax and upregulated Bcl-2 (P < 0.05). TSN IIA has a preventive effect on cerebral infarction by inhibiting neuronal cell apoptosis and inflammatory response in vitro and in vivo.</description><subject>Abietanes - pharmacology</subject><subject>Abietanes - therapeutic use</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cerebral blood flow</subject><subject>Cerebral infarction</subject><subject>Cerebral Infarction - drug therapy</subject><subject>Cerebral Infarction - metabolism</subject><subject>Cerebral Infarction - pathology</subject><subject>DNA nucleotidylexotransferase</subject><subject>Edema</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Flow cytometry</subject><subject>Glucose</subject><subject>Hippocampus</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Ischemia</subject><subject>Lymphocytes B</subject><subject>Male</subject><subject>Neurological diseases</subject><subject>Neurons - drug effects</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Original s</subject><subject>Oxygen</subject><subject>Polymerase chain reaction</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse transcription</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Western blotting</subject><issn>2058-7384</issn><issn>0394-6320</issn><issn>2058-7384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkUtLxTAQhYMoKurelRTcuKlOXk3uRhDxBYIbXYdpm3ojbVKTVvDfm8v1vcpAvjmcOYeQQwqnlCp1BnwhKs4gz8CZEhtkl4HUpeJabP6ad8hBSi8AQIELqek22WFaAKOS7pLuEX1aOh-8LZxfutpNqfB2jsFjXzS27wscwziF5FKBvs1Q1-Mw4BTiexFtGoNPq9XMRlvHvJQJjM3kgi8iTsUQWtvvk60O-2QPPt898nR99Xh5W94_3NxdXtyXI-dsKvmiayTloraUSUsrXrXAZauVRtk0iipLa9C0bZtF3al8PrSoQVEtsNPIGd8j52vdca4H2zbWT9mSGaMbML6bgM78_fFuaZ7Dm5EaKrWQWeDkUyCG19mmyQwurWJAb8OcDNVagcxZ6owe_0NfwhxzbMkwwaSsKi1Wjo5-O_q28lVBBso1kPDZ_khQMKuWzf-W-QcQcJgS</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Zhou, Liang</creator><creator>Zhang, Jie</creator><creator>Wang, Chao</creator><creator>Sun, Qiangsan</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170601</creationdate><title>Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model</title><author>Zhou, Liang ; Zhang, Jie ; Wang, Chao ; Sun, Qiangsan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p332t-39fc5134be125e1636d035d878a5cc717e1b081ddc9bf79460da807184af8a323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Abietanes - pharmacology</topic><topic>Abietanes - therapeutic use</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cerebral blood flow</topic><topic>Cerebral infarction</topic><topic>Cerebral Infarction - drug therapy</topic><topic>Cerebral Infarction - metabolism</topic><topic>Cerebral Infarction - pathology</topic><topic>DNA nucleotidylexotransferase</topic><topic>Edema</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Flow cytometry</topic><topic>Glucose</topic><topic>Hippocampus</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Ischemia</topic><topic>Lymphocytes B</topic><topic>Male</topic><topic>Neurological diseases</topic><topic>Neurons - drug effects</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Original s</topic><topic>Oxygen</topic><topic>Polymerase chain reaction</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse transcription</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Liang</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Sun, Qiangsan</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of immunopathology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Liang</au><au>Zhang, Jie</au><au>Wang, Chao</au><au>Sun, Qiangsan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model</atitle><jtitle>International journal of immunopathology and pharmacology</jtitle><addtitle>Int J Immunopathol Pharmacol</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>30</volume><issue>2</issue><spage>123</spage><epage>129</epage><pages>123-129</pages><issn>2058-7384</issn><issn>0394-6320</issn><eissn>2058-7384</eissn><abstract>We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). In addition, rat primary neuronal cells were isolated and cultured in oxygen-glucose deprivation (OGD) conditions. After pretreatment with TSN, cell viability and apoptosis were observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. The expressions of Bax and B-cell lymphoma 2 (Bcl-2) were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. Compared with untreated cerebral infarction rat, TSN treatment significantly reduced cerebral infarct volume, cerebral edema, and neurological deficits score (P < 0.05). Cell apoptosis as well as the levels of IL-6, TNF-α, and CRP in hippocampus and cortex of cerebral infarction rat were inhibited after pretreatment with TSN (P < 0.05). Furthermore, TSN remarkably increased cell viability and inhibited cell apoptosis ratio (P < 0.05) in OGD-induced rat neuronal cells. Besides, TSN significantly downregulated the expression of Bax and upregulated Bcl-2 (P < 0.05). TSN IIA has a preventive effect on cerebral infarction by inhibiting neuronal cell apoptosis and inflammatory response in vitro and in vivo.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>28402151</pmid><doi>10.1177/0394632017703274</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Abietanes - pharmacology Abietanes - therapeutic use Animals Apoptosis Apoptosis - drug effects Bax protein Bcl-2 protein Brain - drug effects Brain - metabolism Brain - pathology C-reactive protein C-Reactive Protein - metabolism Cell Survival - drug effects Cell viability Cerebral blood flow Cerebral infarction Cerebral Infarction - drug therapy Cerebral Infarction - metabolism Cerebral Infarction - pathology DNA nucleotidylexotransferase Edema Enzyme-linked immunosorbent assay Flow cytometry Glucose Hippocampus Inflammation Interleukin 6 Interleukin-6 - metabolism Ischemia Lymphocytes B Male Neurological diseases Neurons - drug effects Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Original s Oxygen Polymerase chain reaction Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Rats, Sprague-Dawley Reverse transcription Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Western blotting |
| title | Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model |
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