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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

BACKGROUND: The current study was designed to explore the pathway through which adipose-derived mesenchymal stem cells (ADMSCs) affect brain ischemic injury. MATERIAL/METHODS: The improving effect of ADMSCs on the brain function and structure was evaluated in a middle cerebral artery occlusion (MCAO...

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Detalles Bibliográficos
Autores principales: Chi, Lumei, Huang, Yujing, Mao, Ying, Wu, Kunjun, Zhang, Li, Nan, Guangxian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026597/
https://www.ncbi.nlm.nih.gov/pubmed/29888735
http://dx.doi.org/10.12659/MSM.907096
Descripción
Sumario:BACKGROUND: The current study was designed to explore the pathway through which adipose-derived mesenchymal stem cells (ADMSCs) affect brain ischemic injury. MATERIAL/METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.