Tanshinone IIA Pretreatment Protects H9c2 Cells against Anoxia/Reoxygenation Injury: Involvement of the Translocation of Bcl-2 to Mitochondria Mediated by 14-3-3η
Tanshinone IIA is an important component that is isolated from danshen (Salvia miltiorrhiza), which is known to be beneficial for cardiovascular health. In this study, we determined the effects of Tanshinone IIA and its underlying mechanisms of action in an anoxia/reoxygenation (A/R) cell line model...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-13 |
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| creator | He, Ming Xu, Ping Wu, Zelong Huang, Jiyi Qiao, Yang He, Huan Zhang, Zeyu Yin, Dong |
| description | Tanshinone IIA is an important component that is isolated from danshen (Salvia miltiorrhiza), which is known to be beneficial for cardiovascular health. In this study, we determined the effects of Tanshinone IIA and its underlying mechanisms of action in an anoxia/reoxygenation (A/R) cell line model. Prior to inducing A/R injury, rat cardiomyocyte-derived cell line H9c2 was stimulated with 8 μM of Tanshinone IIA for 48 hours. When compared with the A/R group, the Tanshinone IIA treatment significantly increased cell viability and decreased lactate dehydrogenase activity. Tanshinone IIA upregulated 14-3-3η expression and facilitated Bcl-2 translocation to the mitochondrial outer membrane, which bound with voltage-dependent anion channel 1. In addition, pretreatment with Tanshinone IIA reduced the generation of reactive oxygen species and cytochrome c release, inactivated caspase-3, prevented mitochondrial permeability transition pore opening, and reduced the percentage of apoptotic cells. Moreover, treatment with Tanshinone IIA reduced the level of malondialdehyde, thereby increasing the activity of superoxide dismutase and glutathione peroxidase. Silencing the expression of 14-3-3η by adenovirus blocked the above-mentioned results. These novel findings showed that pretreatment with Tanshinone IIA alleviated H9c2 cell damage against A/R injury and was associated with upregulation of 14-3-3η, thereby facilitating Bcl-2 translocation to the mitochondrial outer membrane and preventing mitochondrial permeability transition pore opening, decreasing cytochrome c release, preventing caspase-3 activation, and restraining apoptosis. |
| doi_str_mv | 10.1155/2018/3583921 |
| format | Article |
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In this study, we determined the effects of Tanshinone IIA and its underlying mechanisms of action in an anoxia/reoxygenation (A/R) cell line model. Prior to inducing A/R injury, rat cardiomyocyte-derived cell line H9c2 was stimulated with 8 μM of Tanshinone IIA for 48 hours. When compared with the A/R group, the Tanshinone IIA treatment significantly increased cell viability and decreased lactate dehydrogenase activity. Tanshinone IIA upregulated 14-3-3η expression and facilitated Bcl-2 translocation to the mitochondrial outer membrane, which bound with voltage-dependent anion channel 1. In addition, pretreatment with Tanshinone IIA reduced the generation of reactive oxygen species and cytochrome c release, inactivated caspase-3, prevented mitochondrial permeability transition pore opening, and reduced the percentage of apoptotic cells. Moreover, treatment with Tanshinone IIA reduced the level of malondialdehyde, thereby increasing the activity of superoxide dismutase and glutathione peroxidase. Silencing the expression of 14-3-3η by adenovirus blocked the above-mentioned results. These novel findings showed that pretreatment with Tanshinone IIA alleviated H9c2 cell damage against A/R injury and was associated with upregulation of 14-3-3η, thereby facilitating Bcl-2 translocation to the mitochondrial outer membrane and preventing mitochondrial permeability transition pore opening, decreasing cytochrome c release, preventing caspase-3 activation, and restraining apoptosis.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2018/3583921</identifier><identifier>PMID: 30050654</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>14-3-3 Proteins - metabolism ; Animals ; Apoptosis ; Apoptosis - drug effects ; Bioengineering ; Biological products ; Biological Transport - drug effects ; Biomarkers ; Cardiomyocytes ; Cell culture ; Cell Line ; Cell Survival - drug effects ; Diterpenes, Abietane - therapeutic use ; Enzymes ; Immunoprecipitation ; Ischemia ; L-Lactate Dehydrogenase - metabolism ; Lipid Peroxidation - drug effects ; Medical research ; Microscopy, Confocal ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial Membrane Transport Proteins - drug effects ; Mitochondrial Membrane Transport Proteins - metabolism ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Oxidative stress ; Permeability ; Pharmacology ; Physiology ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rodents</subject><ispartof>Oxidative medicine and cellular longevity, 2018-01, Vol.2018 (2018), p.1-13</ispartof><rights>Copyright © 2018 Zeyu Zhang et al.</rights><rights>Copyright © 2018 Zeyu Zhang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Zeyu Zhang et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-f12de51d4b8b629ee059e65fcc7e32cfab66c33712ae4d1b7b0ff87978a185fa3</citedby><cites>FETCH-LOGICAL-c471t-f12de51d4b8b629ee059e65fcc7e32cfab66c33712ae4d1b7b0ff87978a185fa3</cites><orcidid>0000-0003-1147-903X ; 0000-0002-2869-4521 ; 0000-0002-1007-3583</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046124/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046124/$$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/30050654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Crabtree, Mark</contributor><creatorcontrib>He, Ming</creatorcontrib><creatorcontrib>Xu, Ping</creatorcontrib><creatorcontrib>Wu, Zelong</creatorcontrib><creatorcontrib>Huang, Jiyi</creatorcontrib><creatorcontrib>Qiao, Yang</creatorcontrib><creatorcontrib>He, Huan</creatorcontrib><creatorcontrib>Zhang, Zeyu</creatorcontrib><creatorcontrib>Yin, Dong</creatorcontrib><title>Tanshinone IIA Pretreatment Protects H9c2 Cells against Anoxia/Reoxygenation Injury: Involvement of the Translocation of Bcl-2 to Mitochondria Mediated by 14-3-3η</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Tanshinone IIA is an important component that is isolated from danshen (Salvia miltiorrhiza), which is known to be beneficial for cardiovascular health. 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Moreover, treatment with Tanshinone IIA reduced the level of malondialdehyde, thereby increasing the activity of superoxide dismutase and glutathione peroxidase. Silencing the expression of 14-3-3η by adenovirus blocked the above-mentioned results. These novel findings showed that pretreatment with Tanshinone IIA alleviated H9c2 cell damage against A/R injury and was associated with upregulation of 14-3-3η, thereby facilitating Bcl-2 translocation to the mitochondrial outer membrane and preventing mitochondrial permeability transition pore opening, decreasing cytochrome c release, preventing caspase-3 activation, and restraining apoptosis.</description><subject>14-3-3 Proteins - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bioengineering</subject><subject>Biological products</subject><subject>Biological Transport - drug effects</subject><subject>Biomarkers</subject><subject>Cardiomyocytes</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Diterpenes, Abietane - therapeutic use</subject><subject>Enzymes</subject><subject>Immunoprecipitation</subject><subject>Ischemia</subject><subject>L-Lactate Dehydrogenase - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Ming</au><au>Xu, Ping</au><au>Wu, Zelong</au><au>Huang, Jiyi</au><au>Qiao, Yang</au><au>He, Huan</au><au>Zhang, Zeyu</au><au>Yin, Dong</au><au>Crabtree, Mark</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tanshinone IIA Pretreatment Protects H9c2 Cells against Anoxia/Reoxygenation Injury: Involvement of the Translocation of Bcl-2 to Mitochondria Mediated by 14-3-3η</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Tanshinone IIA is an important component that is isolated from danshen (Salvia miltiorrhiza), which is known to be beneficial for cardiovascular health. In this study, we determined the effects of Tanshinone IIA and its underlying mechanisms of action in an anoxia/reoxygenation (A/R) cell line model. Prior to inducing A/R injury, rat cardiomyocyte-derived cell line H9c2 was stimulated with 8 μM of Tanshinone IIA for 48 hours. When compared with the A/R group, the Tanshinone IIA treatment significantly increased cell viability and decreased lactate dehydrogenase activity. Tanshinone IIA upregulated 14-3-3η expression and facilitated Bcl-2 translocation to the mitochondrial outer membrane, which bound with voltage-dependent anion channel 1. In addition, pretreatment with Tanshinone IIA reduced the generation of reactive oxygen species and cytochrome c release, inactivated caspase-3, prevented mitochondrial permeability transition pore opening, and reduced the percentage of apoptotic cells. Moreover, treatment with Tanshinone IIA reduced the level of malondialdehyde, thereby increasing the activity of superoxide dismutase and glutathione peroxidase. Silencing the expression of 14-3-3η by adenovirus blocked the above-mentioned results. These novel findings showed that pretreatment with Tanshinone IIA alleviated H9c2 cell damage against A/R injury and was associated with upregulation of 14-3-3η, thereby facilitating Bcl-2 translocation to the mitochondrial outer membrane and preventing mitochondrial permeability transition pore opening, decreasing cytochrome c release, preventing caspase-3 activation, and restraining apoptosis.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30050654</pmid><doi>10.1155/2018/3583921</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-1147-903X</orcidid><orcidid>https://orcid.org/0000-0002-2869-4521</orcidid><orcidid>https://orcid.org/0000-0002-1007-3583</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Oxidative medicine and cellular longevity, 2018-01, Vol.2018 (2018), p.1-13 |
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| subjects | 14-3-3 Proteins - metabolism Animals Apoptosis Apoptosis - drug effects Bioengineering Biological products Biological Transport - drug effects Biomarkers Cardiomyocytes Cell culture Cell Line Cell Survival - drug effects Diterpenes, Abietane - therapeutic use Enzymes Immunoprecipitation Ischemia L-Lactate Dehydrogenase - metabolism Lipid Peroxidation - drug effects Medical research Microscopy, Confocal Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Membrane Transport Proteins - drug effects Mitochondrial Membrane Transport Proteins - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Oxidative stress Permeability Pharmacology Physiology Proteins Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Rodents |
| title | Tanshinone IIA Pretreatment Protects H9c2 Cells against Anoxia/Reoxygenation Injury: Involvement of the Translocation of Bcl-2 to Mitochondria Mediated by 14-3-3η |
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