Opioid-induced preconditioning is dependent on caveolin-3 expression.
Opioid-induced preconditioning is dependent on caveolin-3 expression.
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DOI：
10.1213/ane.0b013e3181f3351a
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发表时间：
2010-11
影响因子：
5.7
通讯作者：
Roth DM
中科院分区：
文献类型：
--
作者：
Tsutsumi YM;Kawaraguchi Y;Niesman IR;Patel HH;Roth DM
我们测试的假设，小窝蛋白-3（Cav-3）是必不可少的阿片类药物诱导的预处理在体内。Cav-3过表达小鼠、Cav-3敲除小鼠（Cav-3 KO）和对照在SNC-121（SNC）（δ-选择性阿片激动剂）或纳洛酮（非选择性阿片拮抗剂）存在下暴露于心肌缺血/再灌注（I/R）。SNC保护对照免受I/R损伤。SNC在Cav-3 KO小鼠中不产生保护作用。与对照组相比，Cav-3过表达小鼠表现出对I/R的先天保护，而纳洛酮则消除了这种保护。我们的研究结果表明，阿片诱导的预处理依赖于Cav-3的表达，Cav-3过表达小鼠的内源性保护是阿片依赖性的。
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 (Cav-3 KO), and controls were exposed to myocardial ischemia/reperfusion (I/R) in the presence of SNC-121 (SNC), a delta-selective opioid agonist, or naloxone, a non-selective opioid antagonist. Controls were protected from I/R injury by SNC. No protection was produced by SNC in Cav-3 KO mice. Cav-3 over-expressing mice showed innate protection from I/R compared with controls that was abolished by naloxone. Our results show opioid-induced preconditioning is dependent on Cav-3 expression and endogenous protection in Cav-3 over-expressing mice is opioid dependent.