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诱导耐受性肽诱导海马神经发生,改善狼疮表现。

Induction of hippocampal neurogenesis by a tolerogenic peptide that ameliorates lupus manifestations.

机构信息

Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.

出版信息

J Neuroimmunol. 2011 Mar;232(1-2):151-7. doi: 10.1016/j.jneuroim.2010.11.001. Epub 2010 Dec 3.

DOI:10.1016/j.jneuroim.2010.11.001
PMID:21129786
Abstract

To determine the effect of the tolerogenic peptide hCDR1 on hippocampal neurogenesis, we treated SLE-afflicted (NZBxNZW)F1 mice with hCDR1 (once a week for 10weeks). The treatment resulted in the up-regulation of neurogenesis in the dentate gyrus and restored the NeuN immunoreactivity in brain hippocampi of the mice in association with increased gene expression of IGF-1, NGF and BDNF. Furthermore, hCDR1 treatment significantly up-regulated p-ERK and p-Akt that are suggested to be key components in mediating growth factor-induced neurogenesis. The observed effects of hCDR1 on hippocampal-neurogenesis and on associated signaling pathways suggest a potential role for hCDR1 in CNS lupus.

摘要

为了确定耐受肽 hCDR1 对海马神经发生的影响,我们用 hCDR1 治疗 SLE 发病(NZBxNZW)F1 小鼠(每周一次,共 10 周)。该治疗导致齿状回的神经发生上调,并恢复了与 IGF-1、NGF 和 BDNF 基因表达增加相关的小鼠大脑海马的 NeuN 免疫反应性。此外,hCDR1 治疗显著上调了 p-ERK 和 p-Akt,这被认为是介导生长因子诱导的神经发生的关键成分。hCDR1 对海马神经发生及其相关信号通路的观察到的影响表明 hCDR1 在中枢神经系统狼疮中可能具有作用。

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