Andreia Feital da Costa Pereira, Renan Lage, Mamy Honda Igarashi, Sheila Gomes da Silva, Maurizio Mercuri, Elis Angela de Alcantara Viana, Giulia Okamoto Maciente, Amanda Francielli Pereira, Michelle Sabrina Silva, Gustavo Facchini, Ana Lúcia Alves Tabarini Pinheiro, Samara Eberlin.
Skin aging represents a multifactorial process, progressive and degenerative, of inevitable course, and practically irreversible. The primordial mechanism involved in this process is the excessive production of free radicals, characterizing an oxidative stress environment, after intense exposure of the skin to the various external aggressions and other intrinsic elements. Lipid peroxidation is a consequence of free radicals attack that leads to cell membranes damages. In addition, oxidative stress results in an increase of the glycation process - formation of advanced glycation end products (AGEs), which not only influences the properties of the collagen and extracellular matrix, but also affects the interactions of the cells with the matrix, resulting in cellular alterations, such as migration, growth, proliferation, differentiation, and gene expression. In this study we evaluated the antiaging effectiveness of a cosmetic formulation in the prevention against photodamage caused by UV radiation in human keratinocytes culture. Cells were incubated for 48 hours with three concentrations of the cosmetic formulation previously determined by MTT method and further exposed to a dose of 10 J/cm2 UVA/B radiation. After irradiation, tests systems were incubated with fresh culture medium and maintained for 24 hours for the measurement of the receptor for AGE (rAGE) and lipidic peroxidation by the quantification of malondialdehyde (MDA). As expected, our results demonstrate that UV radiation increase the production of MDA and decrease the amount of free receptor for AGE (rAGEs). However, in comparison to the group only exposed to UV radiation the cosmetic formulation significantly reduces the production of MDA in all evaluated concentrations. Regarding the synthesis of rAGEs, the cosmetic formulation was able to prevent depletion induced by exposure to UV radiation. The results obtained allow us to infer that the cosmetic formulation exerts a protective effect against UV radiation. The mechanisms are not fully elucidated, but it is possible to suggest that an antioxidant action is involved considering the reduction of lipid peroxidation by decreasing the formation of the lipid hydroperoxide malondialdehyde. In addition, the cosmetic formulation demonstrated an anti-glycating action since it increased the amount of free receptor for AGE (rAGEs).