Fig. 1: Psilocin treatment extends cellular lifespan.

Human lung fibroblasts were treated continuously with vehicle (DMSO 0.02%) or 10 µM psilocin until they reached replicative senescence. A Cumulative population doubling curves; arrows indicate time point when cells reach replicative senescence (n = 4 technical replicates). B The area under the curve (AUC) was calculated using the sum of trapeze areas for each time point intervals (n = 4 technical replicates). C Cumulative population doublings at the onset of senescence (n = 4 technical replicates). D Population doubling time comparing young cells (0–4 days) vs. aged cells (60–63 days) post-treatment. Groups were compared using 2-way ANOVA (n = 4 technical replicates). E Cumulative cell number over cellular lifespan. F Table showcasing cellular lifespan population doublings and lifespan extension. Extension refers to the number of additional population doublings of psilocin-treated cells vs. vehicle, which is also shown as a percent increase relative to vehicle-treated cells. G, H Senescence was assessed at 42 days post-treatment by senescence-associated β-galactosidase (β-gal) staining; scale bar = 70 µm (G) and quantitative assessment of β-gal activity (n = 5 technical replicates) (H). I Western blot demonstrating dose-dependent alterations in protein expression of age-associated markers. J Reactive oxygen species (ROS) production was evaluated by Amplex Red assay (n = 3 technical replicates). K Average telomere length was assessed by RT-PCR (n = 4 technical replicates) and is expressed as kilobase pairs per chromosomal end. All values are shown as mean ± SD. Unless otherwise stated, comparisons were made using two-sided unpaired t-tests with unequal variance.; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns not significant.