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Immune Cells in Cancer · Journal article
Cells · September 9, 2026
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This is an in vitro proof-of-concept study developing an H2O2-induced senescence model in adipose-derived mesenchymal stromal cells and demonstrating that fisetin treatment reduces senescence markers (SA-β-gal+ cells and inflammatory cytokines) in cultured cells. The work is mechanistic and descriptive, establishing a platform for testing senotherapeutics rather than demonstrating clinical efficacy.
In vitro cellular model study. Adipose tissue-derived mesenchymal stromal cells (AD-MSCs); specific donor characteristics, passage number, culture conditions, and number of independent replicates not stated.. Intervention: Fisetin treatment (24 h short-term and 7 days long-term); H2O2-induced senescence as the aging model.. Compared with: Non-stimulated AD-MSCs, H2O2-stimulated AD-MSCs (without fisetin), and LPS as an alternative senescence inducer..
SA-β-gal+ cells were 2.0 (0.7)% in non-stimulated AD-MSCs, 81.7 (12.1)% in H2O2-stimulated AD-MSCs, 19.1 (5.2)% after 24 h fisetin treatment, and 13.0 (3.2)% after 7 days fisetin treatment. Fisetin treatment resulted in statistically significant decrease in MCP-1 secretion, especially during long-term incubation. IL-1β showed significant decrease after 7 days of fisetin treatment compared to H2O2.
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This study provides a cellular model for screening senolytic compounds but does not directly inform clinical practice. Fisetin's potential as a senotherapeutic agent requires validation in animal models and clinical trials before therapeutic recommendations can be made.
In vitro mechanistic study establishing a cellular aging model and demonstrating senolytic activity of fisetin in a single-cell system; requires in vivo validation before clinical relevance can be assessed.
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This study provides a cellular model for screening senolytic compounds but does not directly inform clinical practice. Fisetin's potential as a senotherapeutic agent requires validation in animal models and clinical trials before therapeutic recommendations can be made.
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Cellular senescence of adipose tissue-derived mesenchymal stromal cells (AD-MSCs) is associated with chronic low-grade inflammation, metabolic dysfunction, and impaired adipogenesis contributing to the development of obesity, insulin resistance, and the progression of age-associated diseases. The aim of this study was to develop a model of cellular aging based on AD-MSCs to study the senolytic efficacy of the natural fisetin preparation for the subsequent development of geroprotective therapeutic strategies. The senescent markers SA-β-gal, SASP factors, and cell cycle arrest markers p16, p21, and p53 were assessed in models of replicative and stress-induced aging of AD-MSCs. H2O2 was identified as the most effective inducer of AD-MSC cellular senescence in comparison with LPS. It has been shown in the model of H2O2-induced senescence of AD-MSCs that the proportion of SA-β-gal+ cells was 2.0 (0.7)% in non-stimulated AD-MSCs, 81.7 (12.1)% in H2O2-stimulated AD-MSCs, and 19.1 (5.2)% and 13.0 (3.2)% after short-term (24 h) and long-term (7 days) fisetin treatment, respectively, indicating that fisetin treatment was associated with a lower proportion of SA-β-gal+ cells. Fisetin treatment resulted in a statistically significant decrease in the secretion of MCP-1, especially during long-term incubation. IL-1β showed a significant decrease after 7 days of fisetin treatment compared to H2O2, but the effect at 24 h was only significant in the group of 7 days of fisetin treatment. Fisetin treatment was also associated with higher p53 and p21 concentrations. Thus, in the present study, a model of H2O2-induced cellular senescence of AD-MSCs was developed, which can be used to evaluate the geroprotective potential of senotherapeutic preparations; fisetin warrants further evaluation as a potential senotherapeutic agent in this model.
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