Skin aging is characterized by fibroblast senescence, extracellular matrix (ECM) degradation, and impaired wound healing, driven by oxidative stress and telomere dysfunction. Here, we investigated the anti-aging effects of a standardized microwave-assisted propolis extract (MAPE) in both H₂O₂-induced and replicative senescence models of human dermal fibroblasts (HDFs). MAPE significantly reduced reactive oxygen species (ROS) accumulation and enhanced antioxidant gene expression (NQO1, GCLM), indicating activation of NRF2-dependent defense pathways. It suppressed senescence markers (CDKN2A, CDKN1A, IL6), decreased SA-β-gal activity, and attenuated inflammaging. Moreover, MAPE inhibited MMP1 expression, restored COL1A1, and improved fibroblast wound closure, thereby maintaining ECM homeostasis. Importantly, MAPE modulated Wnt/β-catenin signaling by upregulating WNT3A and LEF1 while suppressing DKK1, and increased TERT expression, suggesting involvement of telomerase-related regulatory pathways. These effects resembled those of CHIR99021, a canonical Wnt activator, while providing additional antioxidant protection. Together, our findings suggest that MAPE is a propolis-derived bioactive ingredient that counteracts fibroblast senescence through coordinated modulation of NRF2 and Wnt/β-catenin–TERT signaling pathways, supporting its potential as a cosmeceutical ingredient for mitigating skin aging.

Insufficient sleep can disrupt circadian organization and adversely affect skin condition. Perturbation of the cutaneous clock, which governs skin homeostasis, may contribute to this deterioration. In our study, a six-botanical mixture extract increased PER2 promoter-driven luciferase output in HaCaT keratinocytes, and reduced IL6 and CXCL10 expression, two PER2-associated inflammatory mediators. Separately, a 4-week single-arm pilot study evaluated a cream containing 2.00% (w/w) of a liquid preparation of this extract, applied nightly by 22 women aged 40–70 years with poor sleep quality. Skin indicators, sleep, mood, and salivary melatonin and cortisol were assessed as changes from baseline at week 4. The 13 skin indicators changed from baseline across the anti-aging, barrier, complexion, and dark-circle categories (Cohen’s d 0.47–4.81). Sleep duration increased, whereas PSQI-K and PHQ-9 scores decreased; the melatonin day–night difference increased (d = 0.75); cortisol measures did not change significantly. No adverse skin reactions were reported. These exploratory findings do not establish product-attributable efficacy or a causal PER2-mediated mechanism; placebo, vehicle, expectancy, seasonal, behavioral, and regression-to-the-mean effects cannot be excluded. A randomized, vehicle-controlled study is required, with prespecified primary outcomes, denser circadian sampling, and clock activity measured directly in treated skin.