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Role of decoy molecules in neuronal ischemic preconditioning.

机译:诱饵分子在神经元缺血预处理中的作用。

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AIMS: Decoy receptors bind with TNF related apoptosis inducing ligands (TRAIL) but do not contain the cytoplasmic domains necessary to transduce apoptotic signals. We hypothesized that decoy receptors may confer neuronal protection against lethal ischemia after ischemic preconditioning (IPC). MAIN METHOD: Mixed cortical neurons were exposed to IPC one day prior to TRAIL treatment or lethal ischemia. KEY FINDINGS: IPC increased decoy receptor but reduced death receptor expression compared to lethal ischemia. IPC-induced increase in decoy receptor expression was reduced by prior treatment with CAPE, a nuclear factor-kappa B inhibitor (NFkappaB). SIGNIFICANCE: Expression of decoy molecules, dependent on NFkappaB, may mediate neuronal survival induced by IPC.
机译:目的:诱饵受体与TNF相关的凋亡诱导配体(TRAIL)结合,但不包含转导凋亡信号所必需的胞质域。我们假设在缺血预处理(IPC)后诱饵受体可以赋予神经元保护作用,以抵抗致命性缺血。主要方法:混合皮层神经元在TRAIL治疗或致死性缺血前一天暴露于IPC。主要发现:与致命性缺血相比,IPC增加了诱饵受体但降低了死亡受体的表达。 IPC诱导的诱饵受体表达增加通过预先用核因子-κB抑制剂(NFkappB)进行治疗而减少。意义:依赖NFkappaB诱饵分子的表达可能介导IPC诱导的神经元存活。

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