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首页> 外文期刊>Life sciences >Role of endogenous opioid peptides in protection of ischemic preconditioning in rat small intestine.
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Role of endogenous opioid peptides in protection of ischemic preconditioning in rat small intestine.

机译:内源性阿片肽在大鼠小肠缺血预处理中的保护作用。

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摘要

This study investigated the protective effects of ischemic preconditioning on intestinal ischemic injury and the role of endogenous opioid peptides (EOP) in these effects. Ischemia-reperfusion (I/R) induced by 30-min of ischemia and 60-min of reperfusion significantly increased the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and resulted in serious intestinal edema (wet weight/dry weight). The ischemic preconditioning (PC) elicited by three 8-min occlusion periods interspersed with 10-min reperfusion markedly attenuated intestinal injury caused by ischemia-reperfusion. Pretreatment with morphine (300 microg x kg(-1), i.v.) 10-min before ischemia and reperfusion mimicked the protection produced by PC. Naloxone (3 mg x kg(-1), i.v.) abolished the protection of morphine-induced preconditioning and ischemic preconditioning in rat intestine. However, there were no changes between naloxone alone and control groups. Treatment with naloxone before ischemia-reperfusion had no effect on animals compared with the I/R group. In addition, we also measured the content of endogenous opioid peptides (Leu-enkephalin) in the effluent which was collected before and during preconditioning. It was shown that the release of leu-enkephalin was markedly increased during preconditioning. These results suggested that EOP might play an important role in PC in rat small intestine.
机译:这项研究调查了缺血预处理对肠道缺血性损伤的保护作用,以及内源性阿片肽(EOP)在这些作用中的作用。缺血30分钟和再灌注60分钟引起的缺血再灌注(I / R)显着增加了丙二醛(MDA)和乳酸脱氢酶(LDH)的水平,并导致严重的肠水肿(湿重/干重)。由三个8分钟的闭塞期和10分钟的再灌注引起的缺血预处理(PC)显着减轻了由缺血再灌注引起的肠损伤。在缺血和再灌注前10分钟用吗啡(300 microg x kg(-1),i.v.)进行预处理,模仿了PC产生的保护作用。纳洛酮(3 mg x kg(-1),i.v.)取消了吗啡诱导的大鼠肠道预处理和缺血性预处理的保护作用。但是,单独使用纳洛酮与对照组之间没有变化。与I / R组相比,缺血再灌注前用纳洛酮治疗对动物没有影响。此外,我们还测量了预处理之前和过程中收集的废水中内源性阿片肽(Leu-脑啡肽)的含量。结果表明,在预处理过程中,亮氨酸脑啡肽的释放明显增加。这些结果表明,EOP可能在大鼠小肠的PC中起重要作用。

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