Abstract: Objective: To study the effect and action mechanism of compound collagen peptides powder on chronic skin damage resulting from ultraviolet irradiation in mice. Methods: Female ICR mice were randomly divided into the following groups according to their weights: Normal, model, compound collagen peptides powder, fish collagen peptide. Mice in the model and treatment groups were irradiated on back skin using UV phototherapy apparatus to induce chronic skin damage. During the experiment, the skin appearance of mice was scored each week and photos were taken every 3 weeks. The skin water content was determined by drying method after 9 weeks. The histopathological changes of mice skin were observed using Hematoxylin-Eosin (HE) staining. The total antioxidant capacity (T-AOC) in skin was detected using fluorescene recovery after photobleaching (FRAP). The levels of type I collagen (Col I), elastin (ELN), hyaluronic acid (HA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and advanced glycation end products (AGEs) in the skin were examined using ELISAs. RT-PCR and Western blot analyses were performed to determine the mRNA and protein expression of transforming growth factor β1 (TGF-β1), transforming growth factor β receptor 2 (TGF-βR2), Smad2, Smad3 and Smad7. Results: Compared to the model group, mice in the compound collagen peptides powder group had less wrinkles, no epidermal damage and the skin scores were significantly decreased (P<0.01). The lesions of skin were improved. The water content of skin and T-AOC were significantly increased (P<0.01). The levels of Col I, ELN, HA, GSH-Px, SOD in the skin were significantly increased (P<0.01), whereas MDA and AGEs were significantly decreased (P<0.01). In the skin, the mRNA and protein expression of TGF-β1, TGF-βR2, Smad2, Smad3 were increased (P<0.05), whereas Smad7 was significantly decreased (P<0.01). Conclusion: The compound collagen peptides powder improved the chronic skin damage caused by ultraviolet irradiation. The action mechanism seemed to be related to reduction of oxidative stress, regulation and control signal transduction of TGF-β1/Smads pathway for increasing extracellular matrix synthesis.