ReviewOpen veterinary journal2025
Neuroprotection effect of bovine umbilical mesenchymal stem cell-conditioned medium on the rat model of Alzheimer's disease mediated by upregulation of BDNF and NGF and downregulation of TNF-α and IL-1β.
Review in Open veterinary journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Mesenchymal stem cell application in Alzheimer's disease.Regenerative therapy · 2025Review
- Therapeutic Effects of Intranasal Administration of Mesenchymal Stem Cell-Derived Secretome in Rats Exposed to Chronic Unpredictable Mild Stress.Pharmaceutics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Neurodegenerative diseases (NDDs) are distinguished by impairment and depletion of nerve cells; one of the most common NDDs is Alzheimer's disease (AD), which can appear in early onset or late onset. In recent years, the secretome or conditioned medium of mesenchymal stem cells has provided new hope for improving conditions and preventing AD. One of the secretomes is bovine umbilical mesenchymal stem cells-conditioned medium (BUMSC-CM), where BUMSC is predicted to promote neuronal proliferation potentially. Aim: This study analyzes the therapeutic efficiency of conditioned medium or secretome produced from BUMSC-CM in treating neurodegeneration in animal models of AD. Methods: Five groups consisting of 12 male rats were assigned: untreated (Group A, Results: Our result demonstrated that BUMSC-CM with the dosage of 0.5 ml/kg BW significantly increased BDNF concentration. We also found that BUMSC-CM with dosage 0.2 ml/kg BW and 0.5 ml/kg BW down-regulated IL-1β and TNF-α and upregulated NGF expression. Additionally, the number of neurons in AD rats post-treated with BUMSC-CM was significantly increasing. Furthermore, the amino acids in BUMSC-CM, including isoleucine, leucine, and valine, bind to the amyloid beta protein via interactions that are hydrophobic and hydrogen-bonded. Conclusion: In this study, the neuroprotective potential of BUMSC-CM was demonstrated by its ability to upregulate BDNF and NGF while downregulating IL-1β and TNF-α. Additionally, BUMSC-CM showed potential to promote neuron proliferation in the hippocampus regions of a rat AD model. The main constituents in BUMSC-CM adhere to amyloid beta protein, hence diminishing the likelihood of ND disorders, specifically AD.
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Registered trials
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