hUC-MSCs plus NMN in D-galactose-aged mice and cell senescence models
In D-galactose-induced ageing mice, combined hUC-MSC and NMN treatment showed stronger anti-ageing effects than either alone; cell experiments linked NMN's Nrf2/HO-1 activation to reduced hUC-MSC senescence. [1]
Automatic summary · not editorially reviewed
The key findings
The ageing microenvironment can induce oxidative stress and senescence in transplanted hUC-MSCs, impairing their capacity to delay immunosenescence. [1]
In D-galactose-induced ageing mice, combined hUC-MSC and NMN administration showed enhanced anti-ageing efficacy compared with either treatment alone. [1]
NMN activated the Nrf2/HO-1 pathway, which mitigated hUC-MSC senescence under stress conditions and preserved their anti-ageing properties. [1]
The source at a glance
- Study type / format
- Preclinical study in mice and cells (abstract)
- Population / context
- D-galactose-induced ageing mice and cell senescence models, including hUC-MSCs and lymphocytes
- Summary based on
- Study abstract
- Original publication
- July 28, 2026
Why combine hUC-MSCs with NMN in ageing models
The abstract frames human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) as a promising anti-ageing therapy. It states that the ageing microenvironment can cause oxidative stress and senescence in transplanted hUC-MSCs, impairing their ability to delay immunosenescence. The authors therefore asked whether adding the antioxidant nicotinamide mononucleotide (NMN) would enhance the cells' anti-immunosenescence effects.
Supporting source [1]
Combined treatment in D-galactose-aged mice and cells
Compared with either treatment alone, the combination showed enhanced anti-ageing efficacy in D-galactose-induced ageing mice: marked alleviation of thymic and splenic atrophy, attenuation of body weight loss, and significant improvement in motor and cognitive functions. In cell experiments, combined hUC-MSC and NMN treatment alleviated senescence in lymphocytes while reducing oxidative stress and senescence in hUC-MSCs. Mechanistically, NMN activated the Nrf2/HO-1 pathway, which the authors say mitigated hUC-MSC senescence under stress and preserved their anti-ageing properties.
Supporting source [1]
Abstract-only scope of this preclinical combination study
The abstract reports mouse and cell experiments, not human outcomes, and gives no sample sizes, follow-up durations or effect sizes. It calls the approach promising but does not establish clinical benefit. The full text was not reviewed, so details of design, dosing and statistics remain unknown here.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Mouse and cell experiments, no human outcomes; sample sizes, follow-up and effect sizes are not reported. Findings are associations in preclinical models, not proven clinical benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liu K, Cao Y, Gu Y, Wang Y, Jin L, Liu A, Wang J, Chen S. · europepmc.org · July 28, 2026