Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes
Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study...
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| creator | Mao, Meijiao Zheng, Wang Deng, Bin Wang, Youhua Zhou, Duan Shen, Lin Niku, Wankang Zhang, Na |
| description | Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX. |
| doi_str_mv | 10.1371/journal.pone.0292124 |
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Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0292124</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Aldehydes ; Analysis ; Antimitotic agents ; Antineoplastic agents ; Apoptosis ; Biology and Life Sciences ; Cardiomyocytes ; Cardiotoxicity ; Cell death ; Cinnamaldehyde ; Complications and side effects ; Creatine ; Creatine kinase ; Cytotoxicity ; Doxorubicin ; Experiments ; Ferroptosis ; Fibrosis ; Glutathione ; Health aspects ; Heart cells ; Heme oxygenase (decyclizing) ; Kinases ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Liver cancer ; Medicine and Health Sciences ; Membranes ; Myocardium ; Nuclear transport ; Oxidative stress ; Oxygen ; Patient outcomes ; Reactive oxygen species ; Superoxide ; Superoxide dismutase ; Translocation</subject><ispartof>PloS one, 2023-10, Vol.18 (10), p.e0292124-e0292124</ispartof><rights>COPYRIGHT 2023 Public Library of Science</rights><rights>2023 Mao 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>2023 Mao et al 2023 Mao et al</rights><rights>2023 Mao 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c600t-6af6850735289ec4473852eed883d2702eb7f84ed4f51b4a532970e4bea097403</citedby><cites>FETCH-LOGICAL-c600t-6af6850735289ec4473852eed883d2702eb7f84ed4f51b4a532970e4bea097403</cites><orcidid>0000-0002-7450-7053 ; 0009-0005-4218-819X</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/PMC10569550/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569550/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids></links><search><creatorcontrib>Mao, Meijiao</creatorcontrib><creatorcontrib>Zheng, Wang</creatorcontrib><creatorcontrib>Deng, Bin</creatorcontrib><creatorcontrib>Wang, Youhua</creatorcontrib><creatorcontrib>Zhou, Duan</creatorcontrib><creatorcontrib>Shen, Lin</creatorcontrib><creatorcontrib>Niku, Wankang</creatorcontrib><creatorcontrib>Zhang, Na</creatorcontrib><title>Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes</title><title>PloS one</title><description>Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.</description><subject>Aldehydes</subject><subject>Analysis</subject><subject>Antimitotic agents</subject><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cardiotoxicity</subject><subject>Cell death</subject><subject>Cinnamaldehyde</subject><subject>Complications and side effects</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Cytotoxicity</subject><subject>Doxorubicin</subject><subject>Experiments</subject><subject>Ferroptosis</subject><subject>Fibrosis</subject><subject>Glutathione</subject><subject>Health aspects</subject><subject>Heart cells</subject><subject>Heme oxygenase (decyclizing)</subject><subject>Kinases</subject><subject>L-Lactate 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alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes</title><author>Mao, Meijiao ; Zheng, Wang ; Deng, Bin ; Wang, Youhua ; Zhou, Duan ; Shen, Lin ; Niku, Wankang ; Zhang, Na</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c600t-6af6850735289ec4473852eed883d2702eb7f84ed4f51b4a532970e4bea097403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Aldehydes</topic><topic>Analysis</topic><topic>Antimitotic agents</topic><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Biology and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cardiotoxicity</topic><topic>Cell death</topic><topic>Cinnamaldehyde</topic><topic>Complications and side effects</topic><topic>Creatine</topic><topic>Creatine 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Na</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes</atitle><jtitle>PloS one</jtitle><date>2023-10-12</date><risdate>2023</risdate><volume>18</volume><issue>10</issue><spage>e0292124</spage><epage>e0292124</epage><pages>e0292124-e0292124</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><doi>10.1371/journal.pone.0292124</doi><tpages>e0292124</tpages><orcidid>https://orcid.org/0000-0002-7450-7053</orcidid><orcidid>https://orcid.org/0009-0005-4218-819X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aldehydes Analysis Antimitotic agents Antineoplastic agents Apoptosis Biology and Life Sciences Cardiomyocytes Cardiotoxicity Cell death Cinnamaldehyde Complications and side effects Creatine Creatine kinase Cytotoxicity Doxorubicin Experiments Ferroptosis Fibrosis Glutathione Health aspects Heart cells Heme oxygenase (decyclizing) Kinases L-Lactate dehydrogenase Lactate dehydrogenase Liver cancer Medicine and Health Sciences Membranes Myocardium Nuclear transport Oxidative stress Oxygen Patient outcomes Reactive oxygen species Superoxide Superoxide dismutase Translocation |
| title | Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes |
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