Salvianolic acid B attenuated cisplatin-induced cardiac injury and oxidative stress via modulating Nrf2 signal pathway
Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses ca...
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| Veröffentlicht in: | Journal of toxicological sciences 2021, Vol.46(5), pp.199-207 |
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| creator | Lin, Zhenjian Bao, Yuyan Hong, Bing Wang, Yangyang Zhang, Xiaomin Wu, Yaping |
| description | Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses cardioprotective quality. However, the effect of SalB on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of SalB on cisplatin-induced heart injury. Furthermore, in H9c2 cells, SalB dramatically reduced cisplatin-induced apoptosis and oxidative stress by modulating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. In conclusion, SalB had great potential in mitigating cisplatin-induced cardiac injury. Furthermore, more attention should be placed on natural active compounds containing SalB with antioxidant effects for the treatment of cardiomyopathy. |
| doi_str_mv | 10.2131/jts.46.199 |
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As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses cardioprotective quality. However, the effect of SalB on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of SalB on cisplatin-induced heart injury. Furthermore, in H9c2 cells, SalB dramatically reduced cisplatin-induced apoptosis and oxidative stress by modulating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. In conclusion, SalB had great potential in mitigating cisplatin-induced cardiac injury. Furthermore, more attention should be placed on natural active compounds containing SalB with antioxidant effects for the treatment of cardiomyopathy.</description><identifier>ISSN: 0388-1350</identifier><identifier>EISSN: 1880-3989</identifier><identifier>DOI: 10.2131/jts.46.199</identifier><identifier>PMID: 33952797</identifier><language>eng</language><publisher>Japan: The Japanese Society of Toxicology</publisher><subject>Animals ; Antineoplastic Agents ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Apoptosis ; Benzofurans - pharmacology ; Benzofurans - therapeutic use ; Cancer ; Cardiomyopathy ; Cardiotoxicity ; Cell Line ; Cell Survival - drug effects ; Chemotherapy ; Cisplatin ; Complications ; Creatine Kinase, MB Form - blood ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart Diseases - chemically induced ; Heart Diseases - drug therapy ; Heart Diseases - metabolism ; Heart Diseases - pathology ; Heme Oxygenase-1 - genetics ; Injury prevention ; L-Lactate Dehydrogenase - blood ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium - metabolism ; Myocardium - pathology ; NAD(P)H Dehydrogenase (Quinone) - genetics ; NF-E2-Related Factor 2 - metabolism ; Nrf2 ; Oxidative stress ; Oxidative Stress - drug effects ; Rats ; Salvianolic acid B ; Signal transduction ; Signal Transduction - drug effects ; Stroke Volume - drug effects</subject><ispartof>The Journal of Toxicological Sciences, 2021, Vol.46(5), pp.199-207</ispartof><rights>2021 The Japanese Society of Toxicology</rights><rights>Copyright Japan Science and Technology Agency 2021</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c623t-3b957684ddf884e23eb1010d4a5000a27e55ce5f7387a035f99f6c628b69c48d3</citedby><cites>FETCH-LOGICAL-c623t-3b957684ddf884e23eb1010d4a5000a27e55ce5f7387a035f99f6c628b69c48d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33952797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Zhenjian</creatorcontrib><creatorcontrib>Bao, Yuyan</creatorcontrib><creatorcontrib>Hong, Bing</creatorcontrib><creatorcontrib>Wang, Yangyang</creatorcontrib><creatorcontrib>Zhang, Xiaomin</creatorcontrib><creatorcontrib>Wu, Yaping</creatorcontrib><title>Salvianolic acid B attenuated cisplatin-induced cardiac injury and oxidative stress via modulating Nrf2 signal pathway</title><title>Journal of toxicological sciences</title><addtitle>J Toxicol Sci</addtitle><description>Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses cardioprotective quality. However, the effect of SalB on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of SalB on cisplatin-induced heart injury. Furthermore, in H9c2 cells, SalB dramatically reduced cisplatin-induced apoptosis and oxidative stress by modulating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. In conclusion, SalB had great potential in mitigating cisplatin-induced cardiac injury. Furthermore, more attention should be placed on natural active compounds containing SalB with antioxidant effects for the treatment of cardiomyopathy.</description><subject>Animals</subject><subject>Antineoplastic Agents</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Apoptosis</subject><subject>Benzofurans - pharmacology</subject><subject>Benzofurans - therapeutic use</subject><subject>Cancer</subject><subject>Cardiomyopathy</subject><subject>Cardiotoxicity</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Complications</subject><subject>Creatine Kinase, MB Form - blood</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart Diseases - chemically induced</subject><subject>Heart Diseases - drug therapy</subject><subject>Heart Diseases - metabolism</subject><subject>Heart Diseases - pathology</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Injury prevention</subject><subject>L-Lactate Dehydrogenase - blood</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NAD(P)H Dehydrogenase (Quinone) - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nrf2</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Salvianolic acid B</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stroke Volume - drug effects</subject><issn>0388-1350</issn><issn>1880-3989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1PGzEURS1UBCl0ww9AlrqrNKk_Z-wFCxq1BQnRRenaerE9waPJTLA9afPva0jI6klX5x49XYSuKJkzyunXLqe5qOdU6xM0o0qRimulP6AZ4UpVlEtyjj6m1BHCGiLFGTrnXEvW6GaGtr-h3wYYxj5YDDY4_A1Dzn6YIHuHbUibHnIYqjC4yb4mEF0Ai8PQTXGHYXB4_BdcYbYepxx9SrgI8Xp001tzhR9jy3AKqwF6vIH8_Bd2l-i0hT75T4d7gf78-P60uKsefv28X9w-VLZmPFd8qWVTK-Fcq5TwjPslJZQ4AZIQAqzxUlov24arBgiXrdZtXapqWWsrlOMX6PPeu4njy-RTNt04xfJIMkwyIrlgVBTqy56ycUwp-tZsYlhD3BlKzOvEpkxsRG3KxAW-Piin5dq7I_q-aQFu9kCXMqz8EYCYg-39u0sehMfcPkM0fuD_AVjNjsY</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Lin, Zhenjian</creator><creator>Bao, Yuyan</creator><creator>Hong, Bing</creator><creator>Wang, Yangyang</creator><creator>Zhang, Xiaomin</creator><creator>Wu, Yaping</creator><general>The Japanese Society of Toxicology</general><general>Japan Science and Technology Agency</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>7ST</scope><scope>7U7</scope><scope>C1K</scope><scope>SOI</scope></search><sort><creationdate>20210101</creationdate><title>Salvianolic acid B attenuated cisplatin-induced cardiac injury and oxidative stress via modulating Nrf2 signal pathway</title><author>Lin, Zhenjian ; Bao, Yuyan ; Hong, Bing ; Wang, Yangyang ; Zhang, Xiaomin ; Wu, Yaping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c623t-3b957684ddf884e23eb1010d4a5000a27e55ce5f7387a035f99f6c628b69c48d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antineoplastic Agents</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Apoptosis</topic><topic>Benzofurans - pharmacology</topic><topic>Benzofurans - therapeutic use</topic><topic>Cancer</topic><topic>Cardiomyopathy</topic><topic>Cardiotoxicity</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>Complications</topic><topic>Creatine Kinase, MB Form - blood</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Heart Diseases - chemically induced</topic><topic>Heart Diseases - drug therapy</topic><topic>Heart Diseases - metabolism</topic><topic>Heart Diseases - pathology</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Injury prevention</topic><topic>L-Lactate Dehydrogenase - blood</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>NAD(P)H Dehydrogenase (Quinone) - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nrf2</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Salvianolic acid B</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stroke Volume - drug effects</topic><toplevel>online_resources</toplevel><creatorcontrib>Lin, Zhenjian</creatorcontrib><creatorcontrib>Bao, Yuyan</creatorcontrib><creatorcontrib>Hong, Bing</creatorcontrib><creatorcontrib>Wang, Yangyang</creatorcontrib><creatorcontrib>Zhang, Xiaomin</creatorcontrib><creatorcontrib>Wu, Yaping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><jtitle>Journal of toxicological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Zhenjian</au><au>Bao, Yuyan</au><au>Hong, Bing</au><au>Wang, Yangyang</au><au>Zhang, Xiaomin</au><au>Wu, Yaping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salvianolic acid B attenuated cisplatin-induced cardiac injury and oxidative stress via modulating Nrf2 signal pathway</atitle><jtitle>Journal of toxicological sciences</jtitle><addtitle>J Toxicol Sci</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>46</volume><issue>5</issue><spage>199</spage><epage>207</epage><pages>199-207</pages><issn>0388-1350</issn><eissn>1880-3989</eissn><abstract>Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses cardioprotective quality. However, the effect of SalB on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of SalB on cisplatin-induced heart injury. Furthermore, in H9c2 cells, SalB dramatically reduced cisplatin-induced apoptosis and oxidative stress by modulating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. In conclusion, SalB had great potential in mitigating cisplatin-induced cardiac injury. 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| subjects | Animals Antineoplastic Agents Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Apoptosis Benzofurans - pharmacology Benzofurans - therapeutic use Cancer Cardiomyopathy Cardiotoxicity Cell Line Cell Survival - drug effects Chemotherapy Cisplatin Complications Creatine Kinase, MB Form - blood Heart Heart - drug effects Heart - physiopathology Heart Diseases - chemically induced Heart Diseases - drug therapy Heart Diseases - metabolism Heart Diseases - pathology Heme Oxygenase-1 - genetics Injury prevention L-Lactate Dehydrogenase - blood Male Mice Mice, Inbred C57BL Myocardium - metabolism Myocardium - pathology NAD(P)H Dehydrogenase (Quinone) - genetics NF-E2-Related Factor 2 - metabolism Nrf2 Oxidative stress Oxidative Stress - drug effects Rats Salvianolic acid B Signal transduction Signal Transduction - drug effects Stroke Volume - drug effects |
| title | Salvianolic acid B attenuated cisplatin-induced cardiac injury and oxidative stress via modulating Nrf2 signal pathway |
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