Opioid-Induced Preconditioning Is Dependent on Caveolin-3 Expression
Opioid-Induced Preconditioning Is Dependent on Caveolin-3 Expression
We tested the hypothesis that caveolin-3 (Cav-3) is essential for opioid-induced preconditioning in vivo. Cav-3 overexpressing mice, Cav-3 knockout mice, and controls were exposed to myocardial ischemia/reperfusion (I/R) in the presence of SNC-121 (SNC), a δ-selective opioid agonist, or naloxone, a nonselective opioid antagonist. Controls were protected from I/R injury by SNC. No protection was produced by SNC in Cav-3 knockout mice. Cav-3 overexpressing mice showed innate protection from I/R compared with controls that was abolished by naloxone. Our results show that opioid-induced preconditioning is dependent on Cav-3 expression and that endogenous protection in Cav-3 overexpressing mice is opioid dependent.
- University of Tokushima Japan
- University of California, San Diego United States
Male, Mice, Knockout, Caveolin 3, Naloxone, Myocardium, Narcotic Antagonists, Myocardial Infarction, Blood Pressure, Mice, Transgenic, Myocardial Reperfusion Injury, Drug Administration Schedule, Piperazines, Analgesics, Opioid, Mice, Inbred C57BL, Disease Models, Animal, Mice, Heart Rate, Receptors, Opioid, delta, Benzamides, Animals
Male, Mice, Knockout, Caveolin 3, Naloxone, Myocardium, Narcotic Antagonists, Myocardial Infarction, Blood Pressure, Mice, Transgenic, Myocardial Reperfusion Injury, Drug Administration Schedule, Piperazines, Analgesics, Opioid, Mice, Inbred C57BL, Disease Models, Animal, Mice, Heart Rate, Receptors, Opioid, delta, Benzamides, Animals
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