Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats
Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) i...
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Published in | Oxidative medicine and cellular longevity Vol. 2017; no. 2017; pp. 1 - 18 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
01.01.2017
Hindawi Hindawi Limited |
Subjects | |
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Abstract | Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury. |
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AbstractList | Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury. |
Author | Wang, Shuang-Ran Wang, Hao-Wei Lu, Yan Xu, Wen-Yun Yuan, Hong-Bin Zhang, Hao Sun, Hai-Jing Yang, Feng Fu, Hai-Long Yao, Xue-Ya |
AuthorAffiliation | 5 Hebei North University School of Medicine, Zhangjiakou, Hebei 075000, China 4 Nursing School of Shanghai Jiguang Polytechnic College, No. 2859 Shuichan Road, Shanghai 201901, China 3 Department of Anesthesiology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China 6 School of Pharmacy, Second Military Medical University, No. 325 Guohe Road, Shanghai 200433, China 2 Department of Neurology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China 1 Department of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China |
AuthorAffiliation_xml | – name: 5 Hebei North University School of Medicine, Zhangjiakou, Hebei 075000, China – name: 3 Department of Anesthesiology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China – name: 1 Department of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China – name: 2 Department of Neurology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China – name: 4 Nursing School of Shanghai Jiguang Polytechnic College, No. 2859 Shuichan Road, Shanghai 201901, China – name: 6 School of Pharmacy, Second Military Medical University, No. 325 Guohe Road, Shanghai 200433, China |
Author_xml | – sequence: 1 fullname: Yuan, Hong-Bin – sequence: 2 fullname: Yang, Feng – sequence: 3 fullname: Fu, Hai-Long – sequence: 4 fullname: Xu, Wen-Yun – sequence: 5 fullname: Wang, Shuang-Ran – sequence: 6 fullname: Zhang, Hao – sequence: 7 fullname: Wang, Hao-Wei – sequence: 8 fullname: Lu, Yan – sequence: 9 fullname: Sun, Hai-Jing – sequence: 10 fullname: Yao, Xue-Ya |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28814985$$D View this record in MEDLINE/PubMed |
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Copyright | Copyright © 2017 Hai-Jing Sun et al. Copyright © 2017 Hai-Jing Sun et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2017 Hai-Jing Sun et al. 2017 |
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Snippet | Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study... |
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SubjectTerms | Anesthesiology Animals Apoptosis - drug effects Arachidonic Acids - pharmacology Benzamides - pharmacology Carbamates - pharmacology Cardiology Cardiomyocytes Cells, Cultured Coronary vessels Endocannabinoids - analysis Endocannabinoids - metabolism Fibroblasts Handbooks Hospitals Hypoxia Indoles - pharmacology Ischemia Kinases Laboratory animals Male Malondialdehyde - blood Malondialdehyde - metabolism Myocardial Reperfusion Injury - chemically induced Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Ostomy Pentobarbital - toxicity Peroxidase - blood Peroxidase - metabolism Pharmacology Propofol - pharmacology Propofol - therapeutic use Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Receptor, Cannabinoid, CB1 - antagonists & inhibitors Receptor, Cannabinoid, CB1 - genetics Receptor, Cannabinoid, CB1 - metabolism Receptor, Cannabinoid, CB2 - antagonists & inhibitors Receptor, Cannabinoid, CB2 - genetics Receptor, Cannabinoid, CB2 - metabolism Rodents Signal Transduction - drug effects Superoxide Dismutase - blood Superoxide Dismutase - metabolism Veins & arteries |
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Title | Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats |
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