Afzelin resists UVA damage through autophagy and synergizes with ganoderic acid A to skin photoaging

Feb 10, 2026Phytomedicine : international journal of phytotherapy and phytopharmacology

Afzelin protects skin from UVA damage by promoting cell cleanup and works together with ganoderic acid A against skin aging caused by light

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Abstract

Afzelin restored mitochondrial membrane potential by 2.8-fold in UVA-irradiated human dermal fibroblasts.

Afzelin improved cell viability and decreased markers of senescence, such as β-galactosidase, p53, and p21.
It reduced reactive oxygen species (ROS) levels, indicating a decrease in oxidative stress.
The combination of afzelin and ganoderic acid A (GAA) demonstrated strong synergy in enhancing photoprotection.
In a mouse model, co-treatment with afzelin and GAA led to a ∼37.3% reduction in epidermal thickness.
The treatment also restored collagen I and elastin levels while suppressing p53/p21 expression.

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BACKGROUND: Chronic UVA exposure accelerates photoaging by inducing oxidative stress and mitochondrial dysfunction. Autophagy maintains dermal homeostasis, but its decline promotes aging. Afzelin, a flavonoid with antioxidant activity, has not been fully studied for its autophagy-related photoprotective effects.

PURPOSE: To determine whether afzelin protects against UVA-induced photoaging through autophagy and mitophagy activation, and to assess its synergy with ganoderic acid A (GAA), a triterpenoid possessing established anti-aging activity.

METHODS: UVA-irradiated and D-galactose-induced senescence models of human dermal fibroblasts were examined by Western blotting, immunofluorescence, and flow cytometry. A 20-day UVA mouse model evaluated topical efficacy. Synergy was calculated using the Bliss model.

RESULTS: Afzelin restored UVA-impaired cell viability and reduced β-galactosidase, p53, and p21 while recovering Lamin B1. It lowered ROS levels and restored mitochondrial membrane potential (2.8-fold) via AMPK-AKT/mTOR-ULK1 and PINK1-Parkin activation. Combined with GAA (50 mM), afzelin showed strong synergy (Bliss = 67.6 ± 5.1). In vivo, co-treatment reduced epidermal thickness (∼37.3 %), restored collagen I and elastin, and suppressed p53/p21 expression.

CONCLUSION: Afzelin alleviates UVA-induced photodamage by activating autophagy and mitophagy. Together with the anti-aging triterpenoid GAA, it exerts synergistic anti-photoaging effects, supporting its potential as a natural autophagy-targeting agent for skin rejuvenation.

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Afzelin resists UVA damage through autophagy and synergizes with ganoderic acid A to skin photoaging

Abstract

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