Abstract
Ultraviolet (UV) irradiation, particularly ultraviolet A (UVA), stimulates reactive oxygen species (ROS) production in the epidermis and dermis, which plays a major part in the photoageing of human skin. Several studies have demonstrated that cerium oxide nanoparticles (CeO(2) NP) can exhibit an antioxidant effect and free radical scavenging activity. However, the protective role of CeO(2) NP in skin photoageing and the underlying mechanisms are unclear. In this study, we investigated the effects of CeO(2) NP on UVA-irradiated human skin fibroblasts (HSFs) and explored the potential signalling pathway. CeO(2) NP had no apparent cytotoxicity, and could reduce the production of proinflammatory cytokines, intracellular ROS, senescence-associated β-galactosidase activity, and downregulate phosphorylation of c-Jun N-terminal kinases (JNKs) after exposure to UVA radiation. Based on our findings, CeO(2) NPs have great potential against UVA radiation-induced photoageing in HSFs via regulating the JNK signal-transduction pathway to inhibit oxidative stress and DNA damage.