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首页> 外文期刊>Cellular Physiology and Biochemistry >Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway
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Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

机译：针对缺氧/缺血性损伤的神经保护：δ阿片受体和BDNF-TrkB途径

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The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR’s role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain, we clarified DOR’s specific role in the brain against hypoxic/ischemic injury and reconciled previous controversies in this aspect. Our serial studies have strongly demonstrated that DOR is a unique neuroprotector against hypoxic/ischemic injury in the brain, which has been well confirmed in current research. Moreover, mechanistic studies have shown that during acute phases of hypoxic/ischemic stress, DOR protects the neurons mainly by the stabilization of ionic homeostasis, inhibition of excitatory transmitter release, and attenuation of disrupted neuronal transmission. During prolonged hypoxia/ischemia, however, DOR neuroprotection involves a variety of signaling pathways. More recently, our data suggest that DOR may display its neuroprotective role via the BDNF-TrkB pathway. This review concisely summarizes the progress in this field.
机译：δ阿片受体（DOR）是阿片系统中的三种经典阿片受体之一。传统上认为它主要参与调节疼痛信号通路中的信息传递。尽管对它的其他神经功能的研究还很分散，但是在过去的文献中发现不一致的结果和矛盾的结论，特别是在DOR在缺氧/缺血性脑中的作用方面。从发现that脑比哺乳动物的脑具有更高的DOR密度和对缺氧/缺血性损伤的耐受性这一发现中，我们得到了启发，我们阐明了DOR在脑中针对缺氧/缺血性损伤的特定作用，并在此方面调和了先前的争议。我们的系列研究有力地证明了DOR是针对脑缺氧/缺血性损伤的独特神经保护剂，这一点已在当前研究中得到充分证实。此外，机理研究表明，在缺氧/缺血性应激的急性期，DOR主要通过稳定离子稳态，抑制兴奋性递质释放和减弱神经元传导受阻来保护神经元。然而，在长时间缺氧/缺血期间，DOR神经保护作用涉及多种信号通路。最近，我们的数据表明DOR可能通过BDNF-TrkB途径发挥其神经保护作用。这篇综述简要总结了该领域的进展。

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