Human umbilical cord blood cells rescued traumatic brain injury-induced cardiac and neurological deficits
Hu H., Zhao Q., Liu X., Yan T.
Laboratory Study on Cardiovascular Disease, Chronic Inflammation, published in Ann Transl Med (2020) — 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
- Laboratory Study
- Journal
- Ann Transl Med (2020)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 32355722
- PMCID
- PMC7186665
- DOI
- 10.21037/atm.2020.03.52
- Citations
- 6
Abstract (original English)
Background Traumatic brain injury (TBI) evokes neurological deficits and induces cardiac dysfunction. Treatment with human umbilical cord blood cells (HUCBCs) represents a potential therapeutic strategy for TBI-induced neurological deficits. The present study aimed to determine whether HUCBCs could ameliorate the cardiac dysfunction and neurological deficits induced by TBI. Methods Adult male C57BL/6J mice were subjected to controlled cortical impact (CCI)-induced TBI and were treated with either HUCBCs (1×10 6 ) or phosphate-buffered saline (PBS), via tail vein injections, 3 days after TBI. Neurological and cognitive functions were subsequently evaluated at multiple time points after TBI and cardiac function was assessed by echocardiography 3 and 30 days after TBI. Brain and heart tissues were paraffin-embedded 30 days after TBI. Hematoxylin and eosin (H&E) staining was performed on brain tissue sections to calculate the brain damage volume, and Picro Sirius Red (PSR) staining was performed on heart tissue sections to evaluate myocardial fibrosis. Terminal deoxynucleotide transferase dUTP nick end labeling (TUNEL) staining was employed to assess cell apoptosis 30 days after TBI. Transforming growth factor-beta (TGF-β) and NADPH oxidase-2 (NOX2) levels were assessed to evaluate inflammation and oxidative stress levels 30 days after TBI. Results TBI elicited acute and chronic ca
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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