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缺氧预处理间充质干细胞移植抑制大鼠心脏骤停引起的全脑缺血性脑损伤。

Transplantation with hypoxia-preconditioned mesenchymal stem cells suppresses brain injury caused by cardiac arrest-induced global cerebral ischemia in rats.

机构信息

Department of Intensive Care Unit, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guang Zhou, China.

Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-Sen University, Guang Zhou, China.

出版信息

J Neurosci Res. 2017 Oct;95(10):2059-2070. doi: 10.1002/jnr.24025. Epub 2017 Feb 10.

Abstract

Cardiac arrest-induced global cerebral ischemia is a main cause of neurological dysfunction in emergency medicine. Transplantation with bone marrow mesenchymal stem cells (MSCs) has been used in stroke models to repair the ischemic brain injury, but it is little studied in models with global cerebral ischemia. In the present study, a hypoxia precondition was used to improve the efficacy of MSC transplantation, given the low survival and migration rates and limited differentiation capacities of MSCs. We found that hypoxia can increase the expansion and migration of MSCs by activating the PI3K/AKT and hypoxia-inducible factor-1α/CXC chemokine receptor-4 pathways. By using a cardiac arrest-induced global cerebral ischemic model in rats, we found that transplantation of hypoxia-preconditioned MSCs promoted the migration and integration of MSCs and decreased neuronal death and inflammation in the ischemic cortex. © 2017 Wiley Periodicals, Inc.

摘要

心脏骤停引起的全脑缺血是急诊医学中神经功能障碍的主要原因。骨髓间充质干细胞(MSCs)移植已用于中风模型以修复缺血性脑损伤,但在全脑缺血模型中研究甚少。在本研究中,鉴于 MSC 的低存活率、迁移率和有限的分化能力,采用低氧预处理来提高 MSC 移植的疗效。我们发现低氧通过激活 PI3K/AKT 和低氧诱导因子-1α/CXC 趋化因子受体-4 通路来增加 MSC 的扩增和迁移。通过建立大鼠心脏骤停诱导的全脑缺血模型,我们发现缺氧预处理的 MSC 移植可促进 MSC 的迁移和整合,并减少缺血皮质中的神经元死亡和炎症。© 2017 Wiley Periodicals, Inc.

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