Chronic ultraviolet (UV) exposure is a primary driver of skin photoaging, yet safe and effective natural interventions remain limited. This study investigated the anti-photoaging potential and mechanism of Antarctic krill peptides (AKP), a low-molecular-weight oligopeptide mixture (Mw ~331 Da, with 82.82% <500 Da) prepared by enzymatic hydrolysis and membrane fractionation. AKP exhibited excellent skin permeability in vitro. In UV-irradiated human dermal fibroblasts (HDF), AKP alleviated oxidative damage, restored superoxide dismutase activity, reduced malondialdehyde content, and promoted collagen I and XVII secretion, and inhibited matrix metalloproteinase-1 (MMP-1) expression. In a chronic UV-induced mouse photoaging model, topical AKP ameliorated epidermal thickening, dermal collagen loss, and macroscopic wrinkle formation. Skin proteomics revealed that AKP upregulated estrogen receptor Esr1 and androgen receptor Ar, activating the estrogen signaling pathway, which in turn corrected aberrant keratin (Krt5/14/19) and cell-cycle protein (Cdkn1a/Ccna2) expression. Immunohistochemical validation confirmed that AKP inhibited MMP-1/9 overexpression, elevated tissue inhibitor of metalloproteinase-1 (TIMP-1), and increased deposition of collagens I, III, and XVII, thereby restoring extracellular matrix homeostasis. Collectively, these findings demonstrate that AKP combats skin photoaging through estrogen-mediated regulation of matrix degradation and repair. This work fills a mechanistic gap for Antarctic krill-derived peptides and supports their development as natural marine-based anti-aging agents.

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.

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovitis. The prevalence of RA is estimated to be 0.5–1% worldwide. Methods: This work investigated the therapeutic effects and underlying mechanisms of blue mussel (Mytilus galloprovincialis) oil (BMO) on RA in rats, using green-lipped mussel oil (GMO) and Antarctic krill oil (KO) as controls. Results: The results suggested that BMO, GMO, and KO all alleviated paw swelling in rats and reduced serum levels of rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibody, and pro-inflammatory cytokines such as TNF-$\alpha$ and IL-17. Histopathological assessment further revealed that BMO, GMO, and KO prevented synovial fibroplasia, mitigated inflammatory cell infiltration, and improved cartilage damage in ankle joints. Overall, BMO exhibited slightly superior alleviating effects compared with GMO and KO. Plasma lipidomics analysis revealed that the lipid metabolites altered by BMO showed significant correlations with RA-related indicators, particularly pro-inflammatory cytokines. Functional enrichment analysis suggested the involvement of inflammation-related pathways, particularly the NF-$\kappa$B signaling pathway. Further validation demonstrated that BMO effectively suppressed the production of inflammatory cytokines (TNF-$\alpha$, IL-17) and the expression of NF-$\kappa$B p65, JAK2, and STAT3 proteins in synovial tissue. And IL-17 production in footpad tissues is closely associated with CD3-positive T cells. Similar effects were also observed for GMO and KO. Conclusions: Collectively, BMO might ameliorate RA by inhibiting NF-$\kappa$B and JAK2/STAT3 signaling pathways.