Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways
Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model...
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| Veröffentlicht in: | BioMed research international 2020-01, Vol.2020 (2020), p.1-18 |
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| creator | Liu, Rui Zeng, Li Wang, Yu Wang, Linlin Fang, Jiansong Xing, Jianguo Jiang, Hailun Li, Zhuorong |
| description | Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage. |
| doi_str_mv | 10.1155/2020/5939715 |
| format | Article |
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The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/5939715</identifier><identifier>PMID: 33102583</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antibodies ; Apoptosis ; Binding ; Biomedical research ; c-Jun protein ; Ca2+/calmodulin-dependent protein kinase II ; Calcium ions ; Calcium-binding protein ; Calmodulin ; Cardiomyocytes ; Cytochrome ; Dehydrogenases ; Deprivation ; Glucose ; Heart ; Inflammation ; Injuries ; Ischemia ; JNK protein ; Kinases ; Laboratory animals ; Maintenance ; Mitochondria ; Myocardial ischemia ; NF-κB protein ; Phenolic compounds ; Phenols ; Proteins ; Recovery ; Reperfusion ; Transcription factors ; Tumor necrosis factor-TNF ; Values</subject><ispartof>BioMed research international, 2020-01, Vol.2020 (2020), p.1-18</ispartof><rights>Copyright © 2020 Hailun Jiang et al.</rights><rights>Copyright © 2020 Hailun Jiang 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. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Hailun Jiang et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-5748-7444 ; 0000-0002-8578-0733</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/PMC7568786/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568786/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><contributor>Bhavsar, Pankaj K.</contributor><contributor>Pankaj K Bhavsar</contributor><creatorcontrib>Liu, Rui</creatorcontrib><creatorcontrib>Zeng, Li</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Wang, Linlin</creatorcontrib><creatorcontrib>Fang, Jiansong</creatorcontrib><creatorcontrib>Xing, Jianguo</creatorcontrib><creatorcontrib>Jiang, Hailun</creatorcontrib><creatorcontrib>Li, Zhuorong</creatorcontrib><title>Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways</title><title>BioMed research international</title><description>Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Binding</subject><subject>Biomedical research</subject><subject>c-Jun protein</subject><subject>Ca2+/calmodulin-dependent protein kinase II</subject><subject>Calcium ions</subject><subject>Calcium-binding protein</subject><subject>Calmodulin</subject><subject>Cardiomyocytes</subject><subject>Cytochrome</subject><subject>Dehydrogenases</subject><subject>Deprivation</subject><subject>Glucose</subject><subject>Heart</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Maintenance</subject><subject>Mitochondria</subject><subject>Myocardial ischemia</subject><subject>NF-κB protein</subject><subject>Phenolic compounds</subject><subject>Phenols</subject><subject>Proteins</subject><subject>Recovery</subject><subject>Reperfusion</subject><subject>Transcription factors</subject><subject>Tumor necrosis 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Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways</title><author>Liu, Rui ; Zeng, Li ; Wang, Yu ; Wang, Linlin ; Fang, Jiansong ; Xing, Jianguo ; Jiang, Hailun ; Li, Zhuorong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e298t-d4446b7d2c955ebf5c64254f53ab6416f1a403bbe6923ecf4babca47dac8e9ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Binding</topic><topic>Biomedical research</topic><topic>c-Jun protein</topic><topic>Ca2+/calmodulin-dependent protein kinase II</topic><topic>Calcium ions</topic><topic>Calcium-binding protein</topic><topic>Calmodulin</topic><topic>Cardiomyocytes</topic><topic>Cytochrome</topic><topic>Dehydrogenases</topic><topic>Deprivation</topic><topic>Glucose</topic><topic>Heart</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Maintenance</topic><topic>Mitochondria</topic><topic>Myocardial ischemia</topic><topic>NF-κB protein</topic><topic>Phenolic compounds</topic><topic>Phenols</topic><topic>Proteins</topic><topic>Recovery</topic><topic>Reperfusion</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-TNF</topic><topic>Values</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Rui</creatorcontrib><creatorcontrib>Zeng, Li</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Wang, Linlin</creatorcontrib><creatorcontrib>Fang, Jiansong</creatorcontrib><creatorcontrib>Xing, 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Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways</atitle><jtitle>BioMed research international</jtitle><date>2020-01-01</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>18</epage><pages>1-18</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33102583</pmid><doi>10.1155/2020/5939715</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0001-5748-7444</orcidid><orcidid>https://orcid.org/0000-0002-8578-0733</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Apoptosis Binding Biomedical research c-Jun protein Ca2+/calmodulin-dependent protein kinase II Calcium ions Calcium-binding protein Calmodulin Cardiomyocytes Cytochrome Dehydrogenases Deprivation Glucose Heart Inflammation Injuries Ischemia JNK protein Kinases Laboratory animals Maintenance Mitochondria Myocardial ischemia NF-κB protein Phenolic compounds Phenols Proteins Recovery Reperfusion Transcription factors Tumor necrosis factor-TNF Values |
| title | Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways |
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