Literature DB >> 27855369

Effect of Extracellular Vesicles on Neural Functional Recovery and Immunologic Suppression after Rat Cerebral Apoplexy.

Beilei Hu1, Songfang Chen, Ming Zou, Zhiyong He, Shengmin Shao, Baohua Liu.   

Abstract

BACKGROUND: Previous studies have demonstrated that mesenchymal stem cells (MSCs) can promote the recovery of neural function after cerebral apoplexy by secreting multiple cytokines. In addition, cell factor-derived extracellular vesicles play an important role in recovery of neural function. The aim of this study was to determine the effect of extracellular vesicles on neural functional recovery and brain tissue remodeling after cerebral apoplexy in a rat model.
METHODS: The rat models with local ischemic stroke was established and three random groups were created. In groups A and B, human bone marrow-derived MSCs and MSC-derived extracellular vesicles were transplanted into rats. In the control group (group C), only normal saline was injected. Then, we evaluated motor coordination ability, pathologic changes of the brain, immune responses in the central and peripheral nervous systems, regeneration of blood vessels, and nervous tissue in 4 weeks after cerebral apoplexy.
RESULTS: Obvious regeneration of blood vessels and nervous tissues were identified in groups A and B. There was no significant difference with respect to coordination between groups A and B, but coordination in groups A and B was significantly better than the control group. Immunohistochemical staining of brain tissue showed that extracellular vesicles exerted no effect on infiltration of immune cells in the central nervous system. Weakened immune suppression was noted 1 week after cerebral apoplexy, which provided a favorable environment for remodeling of brain tissue.
CONCLUSION: MSC-derived extracellular vesicles accelerated neural functional recovery after cerebral apoplexy. The weakened immune suppression was beneficial to remodeling of brain tissue.
© 2016 The Author(s) Published by S. Karger AG, Basel.

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Year:  2016        PMID: 27855369     DOI: 10.1159/000452533

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  14 in total

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