RESUMEN
Skin photoageing is a complex, multifactorial process and both intrinsic and extrinsic factors may contribute to its pathogenesis. The ultraviolet-irradiated hairless mouse has been used as an animal model for photoageing, but this model mimics only the 'extrinsic' aspects. Here, we show that skin from old SAMP1 mice, a model for higher oxidative stress and senescence acceleration, exhibited histological and gene expression changes similar to those in human photoaged skin without ultraviolet irradiation. These changes include an increase in elastic fibre and glycosaminoglycan histologically, an upregulation of several proinflammatory cytokines and matrix metalloproteinases, and an increase in lipid peroxide. We propose that SAMP1 mice are a spontaneous animal model for photoageing caused by an exaggerated intrinsic mechanism, namely, higher oxidative status. This mouse model is useful to explore the link between oxidative stress and photoageing, and to evaluate the efficacy of antioxidants.
Asunto(s)
Estrés Oxidativo , Envejecimiento de la Piel/genética , Envejecimiento de la Piel/patología , Animales , Expresión Génica , Interferón gamma/genética , Interleucina-1beta/genética , Interleucina-6/genética , Metaloproteinasa 12 de la Matriz/genética , Metaloproteinasa 7 de la Matriz/genética , Ratones , Modelos Animales , Óxido Nítrico Sintasa de Tipo II/genética , Fenotipo , ARN Mensajero/metabolismo , Envejecimiento de la Piel/fisiología , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Factor de Crecimiento Transformador beta1/genética , Factor de Necrosis Tumoral alfa/genéticaRESUMEN
Components of cherry trees have been used as traditional herbal remedies for various diseases. These components are known to possess antioxidative effects. However, the mechanisms underlying cherry tree component-mediated antioxidative effects remain largely unknown. This study focused on cherry leaves extract (CLE) and examined the mechanism underlying the effect of CLE on tert-butyl hydroperoxide (t-BOOH)-induced melanocytic cell death with DNA damage. Interestingly, CLE prevented t-BOOH-induced cell death with reduction in DNA damage, p38 kinase activation, and reactive oxygen species (ROS) production. CLE-mediated suppression of cell death with reduction of DNA damage, p38 kinase activity and ROS production was prevented by a thioredoxin (Trx) system inhibitor but not by a glutathione (GSH) system inhibitor. Finally, data showed that CLE prevented t-BOOH-induced reduction of Trx2 but not Trx1 and Trx reductases (TrxR1 and TrxR2) protein expression. Thus, our results suggest that CLE prevents t-BOOH-induced reduction in Trx2 expression, promotion of ROS production, activation of p38 kinase, and increase in DNA damage and that it protects against cell death.