Adipose-derived stem cell therapy inhibits the deterioration of cerebral infarction by altering macrophage kinetics.
Tatebayashi K., Takagi T., Fujita M., Doe N., Nakagomi T., Matsuyama T.
Animal Study on Stroke Research, published in Brain Res (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Brain Res (2019)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30721668
- DOI
- 10.1016/j.brainres.2019.01.037
- Citations
- 15
Abstract (original English)
Introduction We previously established a method to isolate and culture human adipose-derived stem cells (hADSCs) using fetal bovine serum and showed the therapeutic impact on cerebral infarction. Recently, we modified the culture method with the use of serum-free media for future clinical applications. This study aims to evaluate whether intravenous administration of hADSCs induced by the serum-free culture method would improve neurobehavioral deficits in mice with cerebral infarction. Results Induced hADSCs possessed the characteristics of mesenchymal stem cells and withstood a freeze-thaw process. hADSC administration improved neurobehavioral deficits in MCAO-treated mice and suppressed brain atrophy at the chronic phase. Although hADSC administration did not affect serum cytokine profiles, it decreased the number of CD11b + monocytes in the spleen. Concomitantly, hADSC administration increased the local accumulation of CD11b + CD163 + M2 macrophages into the border zone of the cerebral infarction at 4 days post-MCAO (the acute phase). Discussion Our data indicate that the systemic administration of hADSCs can improve the neurobehavioral deficits that occur after cerebral infarction by modulating the acute immune response mediated by CD11b + CD163 + M2 macrophages in infarcted lesions.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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