Brain microvascular endothelial cells mediate neuroprotective effects on ischemia/reperfusion neurons
Brain microvascular endothelial cells mediate neuroprotective effects on ischemia/reperfusion neurons
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DOI：
10.1016/j.jep.2010.03.024
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发表时间：
2010-06-16
影响因子：
5.4
通讯作者：
Zhu, Xiaolei
中科院分区：
文献类型：
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作者：
Hua, Qian;Qing, Xuemei;Zhu, Xiaolei
研究目的：血脑屏障（BBB）的通透性是开发新脑病药物的瓶颈，因为药物必须穿过血脑屏障才能发挥治疗作用。为了探索脑部疾病治疗的新途径，本研究探讨脑微血管内皮细胞（MVEC）对损伤神经元的介导作用。材料与方法：培养MVEC和皮质神经元，模拟脑缺血/再灌注（I/R）损伤。然后收集来自四组MVEC的条件培养基——正常细胞（N-CM）、用通络九脑（TLJN）处理的正常细胞（NT-CM）、模拟脑I/R细胞（I/R-CM）和用TLJN处理的模拟细胞（I/RTCM）。将这些条件培养基添加到神经元培养物中，并检查神经元的活力。结果：结果表明，N-CM 可以减轻神经元的 I/R 损伤，并且这种能力可以通过 TLJN 治疗得到改善。然而，I/R-CM会对正常神经元和I/R神经元造成损伤，而I/RT-CM可以显着减轻对I/R神经元的损伤。结论：我们提出MVEC分泌影响神经元存活的活性物质，因此MVEC可能介导对缺血/再灌注神经元的神经保护作用。 (C) 2010 Elsevier Ireland Ltd. 保留所有权利。
Aim of the study: The permeability of the blood-brain barrier (BBB) is a bottleneck for the development of new cerebropathy medications because the medication must be transmitted across the BBB to achieve its curative function. To explore a new approach to the treatment of brain disease, this study investigated the mediating effects of brain microvascular endothelial cells (MVECs) on injured neurons.Materials and methods: MVECs and cortical neurons were cultured and damage by cerebral ischemia/reperfusion (I/R) was simulated. The conditioned media from four groups of MVECs - normal cells (N-CM), normal cells treated with Tong Luo Jiu Nao (TLJN) (NT-CM), simulated cerebral I/R cells (I/R-CM), and simulated cells treated with TLJN (I/RTCM) - were then collected. These conditioned media were added to neuronal cultures and the viability of the neurons was examined.Results: The results demonstrated that N-CM could alleviate I/R damage to neurons, and this capacity could be improved by TLJN treatment. However, I/R-CM could cause damage to normal and I/R neurons, while I/RT-CM could significantly alleviate the damage to I/R neurons.Conclusions: We propose that MVECs secrete active substances that influence the survival of neurons, and so MVECs may mediate a neuroprotective effect on ischemia/reperfusion neurons. (C) 2010 Elsevier Ireland Ltd. All rights reserved.