Conclusion
The efficacy of aspirin for retarding senescence of BM-MSCs was demonstrated. Our study indicated that the mechanisms of this delay might involve influencing immune response and lipid metabolism.
Methods
BM-MSCs were serially passaged to construct a replicative senescence model. SA-β-gal staining, PCR, western blot, and RNA-sequencing were performed on BM-MSCs with or without aspirin treatment, to examine aspirin's impact on bone marrow-derived mesenchymal stem cells.
Results
SA-β-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-β-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment. RNA-sequencing results shown in the biological processes related to aging, aspirin could influence cellular immune response and lipid metabolism.