ArticleAnnals of translational medicine2020
Human umbilical cord blood cells rescued traumatic brain injury-induced cardiac and neurological deficits.
Article in Annals of translational medicine, 2020. 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, 6 citations in OpenAlex.
- Temporal Expression of Neuroinflammatory and Oxidative Stress Markers and Prostaglandin E2 Receptor EP2 Antagonist Effect in a Rat Model of Epileptogenesis.ACS pharmacology & translational science · 2023Article
- The Clinical Differences of Patients With Traumatic Brain Injury in Plateau and Plain Areas.Frontiers in neurology · 2022Article
- Systematic review and meta-analysis of preclinical studies testing mesenchymal stromal cells for traumatic brain injury.NPJ Regenerative medicine · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic 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.
methodsAdult male C57BL/6J mice were subjected to controlled cortical impact (CCI)-induced TBI and were treated with either HUCBCs (1×10
resultsTBI elicited acute and chronic cardiac deficits, identified by decreased left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) values 3 and 30 days after TBI, in addition to neurological and cognitive deficits. TBI mice treated with HUCBCs exhibited enhanced LVEF and FS values 30 days after TBI compared with untreated TBI controls. HUCBC treatment significantly improved neurological and cognitive functions and reduced cardiomyocyte apoptosis, inflammatory response, oxidative stress, and cardiac fibrosis in heart tissues 30 days after TBI.
conclusionsTBI induced both neurological deficits and cardiac dysfunction in mice, which were ameliorated by HUCBC treatment. The anti-inflammatory activities of HUCBCs may contribute to these observed therapeutic effects.
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