ArticleExperimental brain research2023
Human umbilical cord blood mononuclear cells ameliorate ischemic brain injury via promoting microglia/macrophages M2 polarization in MCAO Rats.
Article in Experimental brain research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Nonlinear dose-response of umbilical cord blood IL-6 to severe brain injury in preterm infants: a prospective cohort study.Pediatric research · 2026Article
- Sovateltide at the heart-brain axis crosstalk in Alzheimer's disease: a promising multi-target and cutting-edge therapeutic approach.Inflammopharmacology · 2026Review
- Functional characterization and therapeutic potential of human umbilical cord blood mononuclear cells.Regenerative therapy · 2025Review
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Cerebral infarction is one of the most prevalent cerebrovascular disorders. Microglia and infiltrating macrophages play a key role in regulating the inflammatory response after ischemic stroke. Regulation of microglia/macrophages polarization contributes to the recovery of neurological function in cerebral infarction. In recent decades, human umbilical cord blood mononuclear cells (hUCBMNCs) have been considered a potential therapeutic alternative. However, the mechanism of action is yet unclear. Our study aimed to explore whether hUCBMNCs treatment for cerebral infarction is via regulation of microglia/macrophages polarization. Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) and were treated by intravenous routine with or without hUCBMNCs at 24 h following MCAO. We evaluated the therapeutic effects of hUCBMNCs on cerebral infarction by measuring animal behavior and infarct volume, and further explored the possible mechanisms of hUCBMNCs for cerebral infarction by measuring inflammatory factors and microglia/macrophages markers using Elisa and immunofluorescence staining, respectively. We found that administration with hUCBMNCs improved behavioral functions and reduced infarct volume. Rats treated with hUCBMNCs showed a significant reduction in the level of IL-6, and TNF-α and increased the level of IL-4 and IL-10 compared to those treated without hUCBMNCs. Furthermore, hUCBMNCs inhibited M1 polarization and promoted M2 polarization of microglia/macrophages after MCAO. We conclude that hUCBMNCs could ameliorate cerebral brain injury by promoting microglia/macrophages M2 polarization in MCAO Rats. This experiment provides evidence that hUCBMNCs represent a promising therapeutic option for ischemic stroke.
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