A Collagen-Derived Peptide Fraction CCAP1 from Colla Corii Asini Attenuates UVB-Induced Skin Photoaging via an AMPK-Dependent Nrf2/NF-κB Axis

Chronic UVB exposure drives extrinsic skin aging through oxidative stress, inflammation, and collagen degradation. Although oral collagen peptides are promising photoprotective agents, most preparations lack defined composition and mechanistic validation. Here, we characterized CCAP1, a type I collagen-derived oligopeptide fraction (~1.7 kDa; 94.69% collagen-related components) prepared from Colla Corii Asini by dual-enzymatic hydrolysis and membrane fractionation. In UVB-irradiated mice, oral CCAP1 (100 and 200 mg/kg/d, 28 days) markedly alleviated UVB-induced epidermal hyperplasia, restored skin hydration and dermal collagen types I/III/IV, and suppressed MMP1. Untargeted skin metabolomics nominated AMPK signaling as the central node; Western blotting confirmed that CCAP1 activated the AMPK/Nrf2 axis while suppressing NF-κB phosphorylation, with elevated SOD activity and reduced MDA content. In UVB-injured HaCaT keratinocytes, CCAP1 restored cell viability and reduced intracellular ROS, and both effects were abolished by the AMPK inhibitor Compound C, establishing AMPK as a functionally required mediator. Collectively, CCAP1 is a composition-defined, orally bioavailable collagen peptide fraction that attenuates UVB-induced photoaging via an AMPK-dependent Nrf2/NF-κB regulatory program.