Tail Vein Infusion of Adipose-Derived Mesenchymal Stem Cell Alleviated Inflammatory Response and Improved Blood Brain Barrier Condition by Suppressing Endoplasmic Reticulum Stress in a Middle Cerebral Artery Occlusion Rat Model.

Tail Vein Infusion of Adipose-Derived Mesenchymal Stem Cell Alleviated Inflammatory Response and Improved Blood Brain Barrier Condition by Suppressing Endoplasmic Reticulum Stress in a Middle Cerebral Artery Occlusion Rat Model.
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DOI:
10.12659/msm.907096
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发表时间:
2018-06-11
期刊:
Medical science monitor : international medical journal of experimental and clinical research
影响因子:
--
通讯作者:
Nan G
Nan G
中科院分区:
其他
文献类型:
--
作者:
Chi L;Huang Y;Mao Y;Wu K;Zhang L;Nan G

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本研究旨在探讨脂肪间充质干细胞(adipose-derived mesenchymal stem cells,ADMSCs)对缺血性脑损伤的影响。在大脑中动脉闭塞(MCAO)大鼠模型上评价ADMSCs对脑功能和结构的改善作用。测定脑血屏障(BBB)的通透性、炎症反应和由缺血诱导的内质网(ER)应激相关信号传导。与MCAO组相比,ADMSC的给药降低了神经系统严重程度评分,并限制了脑梗死面积和细胞凋亡。ADMSCs通过降低IL-1β、IL-6和TNF-α的表达抑制脑内炎症反应,从而降低血脑屏障通透性。内质网应激抑制促凋亡因子的表达,诱导抗凋亡因子的表达。ADMSCs通过多种途径影响脑损伤,不仅通过抑制脑梗死区的炎症反应,还通过阻断内质网应激诱导的细胞凋亡。
The current study was designed to explore the pathway through which adipose-derived mesenchymal stem cells (ADMSCs) affect brain ischemic injury. The improving effect of ADMSCs on the brain function and structure was evaluated in a middle cerebral artery occlusion (MCAO) rat model. The permeability of the brain-blood barrier (BBB), inflammatory response, and endoplasmic reticulum (ER) stress-related signaling induced by ischemia were determined. The administration of ADMSCs decreased neurological severity score when compared with that in the MCAO group and also restricted the brain infarction area as well as cell apoptosis. ADMSCs suppressed the inflammation in brains by decreasing the expressions of IL-1β, IL-6, and TNF-α, contributing to the decreased permeability of the BBB. The expressions of pro-apoptosis factors in ER stress were inhibited while that of anti-apoptosis factors were induced. ADMSCs affected brain injury in multiple ways, not only by suppressing inflammation in the brain infarction area, but also by blocking ER stress-induced apoptosis.