Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart
Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear. In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of A...
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| Veröffentlicht in: | Phytomedicine (Stuttgart) 2017-10, Vol.34, p.106-114 |
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| creator | Yuan, Yong Cao, Wenjiang Hong, Ye Guo, Xinhong Wang, Yanfang Wang, Yangyang Wang, Xinchun Hu, Ping |
| description | Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear.
In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca2+ and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm.
In conclusion, the study suggests that Tilianin may be of clinical value for the protective effects of cardiomyocytes and mitochondria by inhibiting myocardium energy metabolism and apoptosis during myocardial ischemia-reperfusion injury (MIRI).
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| doi_str_mv | 10.1016/j.phymed.2017.08.007 |
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In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca2+ and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm.
In conclusion, the study suggests that Tilianin may be of clinical value for the protective effects of cardiomyocytes and mitochondria by inhibiting myocardium energy metabolism and apoptosis during myocardial ischemia-reperfusion injury (MIRI).
[Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2017.08.007</identifier><identifier>PMID: 28899492</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>Adenosine Triphosphatases - metabolism ; Animals ; Apoptosis ; Apoptosis - drug effects ; Caspase 3 - metabolism ; Cell Line ; Energy Metabolism ; Flavonoids - pharmacology ; Glycosides - pharmacology ; Heart - drug effects ; Mechanisms ; Mitochondria ; Mitochondria, Heart - drug effects ; MRI ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - metabolism ; Myocytes, Cardiac - drug effects ; Protective effect ; Rats ; Reactive Oxygen Species - metabolism ; Tilianin</subject><ispartof>Phytomedicine (Stuttgart), 2017-10, Vol.34, p.106-114</ispartof><rights>2017 Elsevier GmbH</rights><rights>Copyright © 2017 Elsevier GmbH. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-78bc0fe5f75eff4c2fcf11c949fb4bda61fd5a0513f884f8c0fa7c58924124a33</citedby><cites>FETCH-LOGICAL-c362t-78bc0fe5f75eff4c2fcf11c949fb4bda61fd5a0513f884f8c0fa7c58924124a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.phymed.2017.08.007$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28899492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Yong</creatorcontrib><creatorcontrib>Cao, Wenjiang</creatorcontrib><creatorcontrib>Hong, Ye</creatorcontrib><creatorcontrib>Guo, Xinhong</creatorcontrib><creatorcontrib>Wang, Yanfang</creatorcontrib><creatorcontrib>Wang, Yangyang</creatorcontrib><creatorcontrib>Wang, Xinchun</creatorcontrib><creatorcontrib>Hu, Ping</creatorcontrib><title>Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear.
In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca2+ and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm.
In conclusion, the study suggests that Tilianin may be of clinical value for the protective effects of cardiomyocytes and mitochondria by inhibiting myocardium energy metabolism and apoptosis during myocardial ischemia-reperfusion injury (MIRI).
[Display omitted]</description><subject>Adenosine Triphosphatases - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Line</subject><subject>Energy Metabolism</subject><subject>Flavonoids - pharmacology</subject><subject>Glycosides - pharmacology</subject><subject>Heart - drug effects</subject><subject>Mechanisms</subject><subject>Mitochondria</subject><subject>Mitochondria, Heart - drug effects</subject><subject>MRI</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Protective effect</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Tilianin</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFq3DAURUVJaSZp_6AEL7Ox8yTLtrwplJC2gUA2KXQnNPITo8GWHEkemEX_vTJOtl09JJ2rxz2EfKVQUaDt3bGaD-cJh4oB7SoQFUD3gexoS0UJffPnguyg57zsKK0vyVWMRwDK-w4-kUsmRN_znu3I3xc7WuWsK-aAKaBKE7q0Hk55xmI6e63CYNVY2KgPOFlVBpwxmCVa7wrrjks4Fyer1kzEcFJpvfemmGzy-uDdENa0WZxOW6IIKhUHVCF9Jh-NGiN-eZvX5PePh5f7X-XT88_H--9Ppa5blspO7DUYbEzXoDFcM6MNpTo3MHu-H1RLzdAoaGhthOBGZFh1uhE945RxVdfX5Hb7dw7-dcGY5JTb4Dgqh36Jkva1aIEBExnlG6qDjzGgkXOwkwpnSUGu4uVRbuLlKl6CkFl8jt28bVj269t76N10Br5tAOaeJ4tBRm3RaRxsQJ3k4O3_N_wDrGCbKw</recordid><startdate>20171015</startdate><enddate>20171015</enddate><creator>Yuan, Yong</creator><creator>Cao, Wenjiang</creator><creator>Hong, Ye</creator><creator>Guo, Xinhong</creator><creator>Wang, Yanfang</creator><creator>Wang, Yangyang</creator><creator>Wang, Xinchun</creator><creator>Hu, Ping</creator><general>Elsevier GmbH</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></search><sort><creationdate>20171015</creationdate><title>Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart</title><author>Yuan, Yong ; Cao, Wenjiang ; Hong, Ye ; Guo, Xinhong ; Wang, Yanfang ; Wang, Yangyang ; Wang, Xinchun ; Hu, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-78bc0fe5f75eff4c2fcf11c949fb4bda61fd5a0513f884f8c0fa7c58924124a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine Triphosphatases - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Line</topic><topic>Energy Metabolism</topic><topic>Flavonoids - pharmacology</topic><topic>Glycosides - pharmacology</topic><topic>Heart - drug effects</topic><topic>Mechanisms</topic><topic>Mitochondria</topic><topic>Mitochondria, Heart - drug effects</topic><topic>MRI</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - metabolism</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Protective effect</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tilianin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Yong</creatorcontrib><creatorcontrib>Cao, Wenjiang</creatorcontrib><creatorcontrib>Hong, Ye</creatorcontrib><creatorcontrib>Guo, Xinhong</creatorcontrib><creatorcontrib>Wang, Yanfang</creatorcontrib><creatorcontrib>Wang, Yangyang</creatorcontrib><creatorcontrib>Wang, Xinchun</creatorcontrib><creatorcontrib>Hu, Ping</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>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Yong</au><au>Cao, Wenjiang</au><au>Hong, Ye</au><au>Guo, Xinhong</au><au>Wang, Yanfang</au><au>Wang, Yangyang</au><au>Wang, Xinchun</au><au>Hu, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2017-10-15</date><risdate>2017</risdate><volume>34</volume><spage>106</spage><epage>114</epage><pages>106-114</pages><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear.
In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca2+ and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm.
In conclusion, the study suggests that Tilianin may be of clinical value for the protective effects of cardiomyocytes and mitochondria by inhibiting myocardium energy metabolism and apoptosis during myocardial ischemia-reperfusion injury (MIRI).
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| subjects | Adenosine Triphosphatases - metabolism Animals Apoptosis Apoptosis - drug effects Caspase 3 - metabolism Cell Line Energy Metabolism Flavonoids - pharmacology Glycosides - pharmacology Heart - drug effects Mechanisms Mitochondria Mitochondria, Heart - drug effects MRI Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - prevention & control Myocardium - metabolism Myocytes, Cardiac - drug effects Protective effect Rats Reactive Oxygen Species - metabolism Tilianin |
| title | Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart |
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