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Table · dataset · 2026

Supplementary file 1_Formononetin improved healthspan via the P53/P21/CDK4 pathway in SAMP8 mice and DAF-16/SKN-1 signaling pathway in C.elegans.docx

Listed in figshare and Loughborough Research Repository — shown once because both records carry DOI 10.3389/fphar.2026.1918524.s001

Objective<p>To investigate the healthy aging effects of Formononetin and its underlying molecular mechanisms.</p>Methods<p>SAMP8 mice were administered Formononetin (4, 8, 16 mg/kg, po) for 5 months.

Description

Behavioral tests were performed in 9-month-old mice, followed by histopathology. 5-methylcytosine (5-mC) level in the brain were detected by immunofluorescence, aging-related protein expression was measured by Western blot.

In C. elegans, the lifespan, stress resistance, and aging-related gene expressions were assessed. Mutant strains (daf-16 and skn-1) were used to verify pathway dependency.</p>Results<p>Formononetin dose-dependently ameliorated cognitive deficits, anxiety-like behaviors, and motor decline in SAMP8 mice, attenuated neuronal damage in the hippocampal CA1, DG and cerebral cortex, reversed 5-mC level, downregulated protein expression of P53, P21, while upregulated CDK4 and Nrf2.

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In C. elegans, Formononetin (37.30 μmol/L) significantly extended lifespan under normal, thermal stress, and oxidative stress conditions, improved locomotion, reduced lipofuscin accumulation, increased total SOD activity, and upregulated skn-1, sir-2.1, daf-16 and sod-3 mRNA. No lifespan extension was observed in daf-16 or skn-1 mutants.</p>Conclusion<p>Formononetin effectively attenuated cognitive deficits, ameliorated neuronal damage and increased 5-mC level, possibly via regulated P53, P21, CDK4 and Nrf2 protein expression in the brain of SAMP8 mice.

In C. elegans, Formononetin extended lifespan, increased stress resistance, and improved locomotion and lipofuscin accumulation, possibly via regulated expression of DAF-16 and SKN-1.</p>

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