Melatonin provides protection against heat stroke‐induced myocardial injury in male rats
Objectives This study aimed to investigate the cardioprotective effects of melatonin on heat stroke (HS) induced acute myocardial infarction in rats and to explore the underlying mechanisms. Methods Myocardial injury was induced by subjecting the anaesthetized rats to a high ambient temperature of 4...
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| Veröffentlicht in: | Journal of pharmacy and pharmacology 2018-06, Vol.70 (6), p.760-767 |
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| container_title | Journal of pharmacy and pharmacology |
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| creator | Lin, Xiaojing Zhao, Tingbao Lin, Cheng‐Hsien Zuo, Dan Ye, Zhujun Lin, Shide Wen, Shaonan Liu, Lin Lin, Mao‐Tsun Chang, Ching‐Ping Chao, Chien‐Ming |
| description | Objectives
This study aimed to investigate the cardioprotective effects of melatonin on heat stroke (HS) induced acute myocardial infarction in rats and to explore the underlying mechanisms.
Methods
Myocardial injury was induced by subjecting the anaesthetized rats to a high ambient temperature of 43°C for 70 min. Such a high ambient temperature caused hyperthermia, hypotension and myocardial injury in rats. Rats were treated with melatonin (3 mg/kg) intravenously one hour before and followed by an additional dose immediately after heat stress.
Key findings
At the onset of HS, animals displayed myocardial injury evidenced by increased levels of cardiac damage indicators (e.g. total lactate dehydrogenase, cardiac troponin I and creatine kinase‐MB), increased cardiac damage scores and suppressed left ventricular performance. Animals with HS also had increased cardiac oxidative stress evidenced by increased levels of lipid peroxidation (e.g. increased thiobarbituric acid reactive substances) and decreased levels of antioxidant enzymes (e.g. superoxide dismutase, catalase and reduced glutathione) and activated inflammation (e.g. increased levels of interleukin‐6 and tumour necrosis factor‐α). Pretreatment with melatonin significantly reversed the HS‐induced myocardial injury, cardiac oxidative stress and cardiac inflammation.
Conclusions
Melatonin may protect against HS‐induced myocardial injury in male rats by mitigating oxidative stress and inflammation. |
| doi_str_mv | 10.1111/jphp.12895 |
| format | Article |
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This study aimed to investigate the cardioprotective effects of melatonin on heat stroke (HS) induced acute myocardial infarction in rats and to explore the underlying mechanisms.
Methods
Myocardial injury was induced by subjecting the anaesthetized rats to a high ambient temperature of 43°C for 70 min. Such a high ambient temperature caused hyperthermia, hypotension and myocardial injury in rats. Rats were treated with melatonin (3 mg/kg) intravenously one hour before and followed by an additional dose immediately after heat stress.
Key findings
At the onset of HS, animals displayed myocardial injury evidenced by increased levels of cardiac damage indicators (e.g. total lactate dehydrogenase, cardiac troponin I and creatine kinase‐MB), increased cardiac damage scores and suppressed left ventricular performance. Animals with HS also had increased cardiac oxidative stress evidenced by increased levels of lipid peroxidation (e.g. increased thiobarbituric acid reactive substances) and decreased levels of antioxidant enzymes (e.g. superoxide dismutase, catalase and reduced glutathione) and activated inflammation (e.g. increased levels of interleukin‐6 and tumour necrosis factor‐α). Pretreatment with melatonin significantly reversed the HS‐induced myocardial injury, cardiac oxidative stress and cardiac inflammation.
Conclusions
Melatonin may protect against HS‐induced myocardial injury in male rats by mitigating oxidative stress and inflammation.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/jphp.12895</identifier><identifier>PMID: 29484657</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animals ; Antioxidants ; Calcium-binding protein ; Catalase ; Cerebral infarction ; circulatory failure ; Creatine ; Creatine kinase ; Glutathione ; Heart ; Heart diseases ; Heat ; Heat stress ; Heat stroke ; Heat tolerance ; Heatstroke ; Hyperthermia ; Hypotension ; Inflammation ; L-Lactate dehydrogenase ; Lactic acid ; Lipid peroxidation ; Melatonin ; Myocardial infarction ; Oxidative stress ; Peroxidation ; Rats ; Rodents ; Superoxide dismutase ; Thiobarbituric acid ; Troponin ; Troponin I ; Tumors ; Ventricle</subject><ispartof>Journal of pharmacy and pharmacology, 2018-06, Vol.70 (6), p.760-767</ispartof><rights>2018 Royal Pharmaceutical Society</rights><rights>2018 Royal Pharmaceutical Society.</rights><rights>Copyright © 2018 Royal Pharmaceutical Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3575-1e1fd76d44a062bdf05a02778feaa23f67fb5a3c0ef38ddbe06060f96a23fd3</citedby><cites>FETCH-LOGICAL-c3575-1e1fd76d44a062bdf05a02778feaa23f67fb5a3c0ef38ddbe06060f96a23fd3</cites><orcidid>0000-0003-0890-9414</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjphp.12895$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjphp.12895$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27933,27934,45583,45584</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29484657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Xiaojing</creatorcontrib><creatorcontrib>Zhao, Tingbao</creatorcontrib><creatorcontrib>Lin, Cheng‐Hsien</creatorcontrib><creatorcontrib>Zuo, Dan</creatorcontrib><creatorcontrib>Ye, Zhujun</creatorcontrib><creatorcontrib>Lin, Shide</creatorcontrib><creatorcontrib>Wen, Shaonan</creatorcontrib><creatorcontrib>Liu, Lin</creatorcontrib><creatorcontrib>Lin, Mao‐Tsun</creatorcontrib><creatorcontrib>Chang, Ching‐Ping</creatorcontrib><creatorcontrib>Chao, Chien‐Ming</creatorcontrib><title>Melatonin provides protection against heat stroke‐induced myocardial injury in male rats</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives
This study aimed to investigate the cardioprotective effects of melatonin on heat stroke (HS) induced acute myocardial infarction in rats and to explore the underlying mechanisms.
Methods
Myocardial injury was induced by subjecting the anaesthetized rats to a high ambient temperature of 43°C for 70 min. Such a high ambient temperature caused hyperthermia, hypotension and myocardial injury in rats. Rats were treated with melatonin (3 mg/kg) intravenously one hour before and followed by an additional dose immediately after heat stress.
Key findings
At the onset of HS, animals displayed myocardial injury evidenced by increased levels of cardiac damage indicators (e.g. total lactate dehydrogenase, cardiac troponin I and creatine kinase‐MB), increased cardiac damage scores and suppressed left ventricular performance. Animals with HS also had increased cardiac oxidative stress evidenced by increased levels of lipid peroxidation (e.g. increased thiobarbituric acid reactive substances) and decreased levels of antioxidant enzymes (e.g. superoxide dismutase, catalase and reduced glutathione) and activated inflammation (e.g. increased levels of interleukin‐6 and tumour necrosis factor‐α). Pretreatment with melatonin significantly reversed the HS‐induced myocardial injury, cardiac oxidative stress and cardiac inflammation.
Conclusions
Melatonin may protect against HS‐induced myocardial injury in male rats by mitigating oxidative stress and inflammation.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Calcium-binding protein</subject><subject>Catalase</subject><subject>Cerebral infarction</subject><subject>circulatory failure</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Glutathione</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heat</subject><subject>Heat stress</subject><subject>Heat stroke</subject><subject>Heat tolerance</subject><subject>Heatstroke</subject><subject>Hyperthermia</subject><subject>Hypotension</subject><subject>Inflammation</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Lipid peroxidation</subject><subject>Melatonin</subject><subject>Myocardial infarction</subject><subject>Oxidative stress</subject><subject>Peroxidation</subject><subject>Rats</subject><subject>Rodents</subject><subject>Superoxide dismutase</subject><subject>Thiobarbituric acid</subject><subject>Troponin</subject><subject>Troponin I</subject><subject>Tumors</subject><subject>Ventricle</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kM1KxDAUhYMozji68QGk4EaEjmnaJu1SBnWUEQd05aakzY2T2p8xaZXufASf0ScxtaMLF967OBfux-FwEDr08NSzc5avV-upR6I43EJjggPiMi-MttEYY0JcP2T-CO0Zk2OMGaV0F41IHEQBDdkYPd5CwZu6UpWz1vWrEmD6o4GsUXXl8CeuKtM4K-CNYxpdP8Pn-4eqRJuBcMquzrgWiheOqvJWd1ackhfgaN6YfbQjeWHgYKMTdH958TCbu4u7q-vZ-cLNbLTQ9cCTglERBBxTkgqJQ44JY5EEzokvKZNpyP0Mg_QjIVLA1K6Maf8U_gSdDK429UsLpklKZTIoCl5B3ZqEYBxFUUwZtujxHzSvW13ZbJbyQxrQIPYtdTpQma6N0SCTtVYl113i4aTvO-n7Tr77tvDRxrJNSxC_6E_BFvAG4E0V0P1jldws58vB9AvDMI1F</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Lin, Xiaojing</creator><creator>Zhao, Tingbao</creator><creator>Lin, Cheng‐Hsien</creator><creator>Zuo, Dan</creator><creator>Ye, Zhujun</creator><creator>Lin, Shide</creator><creator>Wen, Shaonan</creator><creator>Liu, Lin</creator><creator>Lin, Mao‐Tsun</creator><creator>Chang, Ching‐Ping</creator><creator>Chao, Chien‐Ming</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0890-9414</orcidid></search><sort><creationdate>201806</creationdate><title>Melatonin provides protection against heat stroke‐induced myocardial injury in male rats</title><author>Lin, Xiaojing ; Zhao, Tingbao ; Lin, Cheng‐Hsien ; Zuo, Dan ; Ye, Zhujun ; Lin, Shide ; Wen, Shaonan ; Liu, Lin ; Lin, Mao‐Tsun ; Chang, Ching‐Ping ; Chao, Chien‐Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3575-1e1fd76d44a062bdf05a02778feaa23f67fb5a3c0ef38ddbe06060f96a23fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Calcium-binding protein</topic><topic>Catalase</topic><topic>Cerebral infarction</topic><topic>circulatory failure</topic><topic>Creatine</topic><topic>Creatine kinase</topic><topic>Glutathione</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heat</topic><topic>Heat stress</topic><topic>Heat stroke</topic><topic>Heat tolerance</topic><topic>Heatstroke</topic><topic>Hyperthermia</topic><topic>Hypotension</topic><topic>Inflammation</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Lipid peroxidation</topic><topic>Melatonin</topic><topic>Myocardial infarction</topic><topic>Oxidative stress</topic><topic>Peroxidation</topic><topic>Rats</topic><topic>Rodents</topic><topic>Superoxide dismutase</topic><topic>Thiobarbituric acid</topic><topic>Troponin</topic><topic>Troponin I</topic><topic>Tumors</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Xiaojing</creatorcontrib><creatorcontrib>Zhao, Tingbao</creatorcontrib><creatorcontrib>Lin, Cheng‐Hsien</creatorcontrib><creatorcontrib>Zuo, Dan</creatorcontrib><creatorcontrib>Ye, Zhujun</creatorcontrib><creatorcontrib>Lin, Shide</creatorcontrib><creatorcontrib>Wen, Shaonan</creatorcontrib><creatorcontrib>Liu, Lin</creatorcontrib><creatorcontrib>Lin, Mao‐Tsun</creatorcontrib><creatorcontrib>Chang, Ching‐Ping</creatorcontrib><creatorcontrib>Chao, Chien‐Ming</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Xiaojing</au><au>Zhao, Tingbao</au><au>Lin, Cheng‐Hsien</au><au>Zuo, Dan</au><au>Ye, Zhujun</au><au>Lin, Shide</au><au>Wen, Shaonan</au><au>Liu, Lin</au><au>Lin, Mao‐Tsun</au><au>Chang, Ching‐Ping</au><au>Chao, Chien‐Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Melatonin provides protection against heat stroke‐induced myocardial injury in male rats</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2018-06</date><risdate>2018</risdate><volume>70</volume><issue>6</issue><spage>760</spage><epage>767</epage><pages>760-767</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><abstract>Objectives
This study aimed to investigate the cardioprotective effects of melatonin on heat stroke (HS) induced acute myocardial infarction in rats and to explore the underlying mechanisms.
Methods
Myocardial injury was induced by subjecting the anaesthetized rats to a high ambient temperature of 43°C for 70 min. Such a high ambient temperature caused hyperthermia, hypotension and myocardial injury in rats. Rats were treated with melatonin (3 mg/kg) intravenously one hour before and followed by an additional dose immediately after heat stress.
Key findings
At the onset of HS, animals displayed myocardial injury evidenced by increased levels of cardiac damage indicators (e.g. total lactate dehydrogenase, cardiac troponin I and creatine kinase‐MB), increased cardiac damage scores and suppressed left ventricular performance. Animals with HS also had increased cardiac oxidative stress evidenced by increased levels of lipid peroxidation (e.g. increased thiobarbituric acid reactive substances) and decreased levels of antioxidant enzymes (e.g. superoxide dismutase, catalase and reduced glutathione) and activated inflammation (e.g. increased levels of interleukin‐6 and tumour necrosis factor‐α). Pretreatment with melatonin significantly reversed the HS‐induced myocardial injury, cardiac oxidative stress and cardiac inflammation.
Conclusions
Melatonin may protect against HS‐induced myocardial injury in male rats by mitigating oxidative stress and inflammation.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29484657</pmid><doi>10.1111/jphp.12895</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-0890-9414</orcidid></addata></record> |
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| ispartof | Journal of pharmacy and pharmacology, 2018-06, Vol.70 (6), p.760-767 |
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| subjects | Animals Antioxidants Calcium-binding protein Catalase Cerebral infarction circulatory failure Creatine Creatine kinase Glutathione Heart Heart diseases Heat Heat stress Heat stroke Heat tolerance Heatstroke Hyperthermia Hypotension Inflammation L-Lactate dehydrogenase Lactic acid Lipid peroxidation Melatonin Myocardial infarction Oxidative stress Peroxidation Rats Rodents Superoxide dismutase Thiobarbituric acid Troponin Troponin I Tumors Ventricle |
| title | Melatonin provides protection against heat stroke‐induced myocardial injury in male rats |
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