Preclinical evaluation of an antiaging cosmetic in the prevention of glycation and lipid peroxidation
Author: Samara Eberlin
Published at: September 18, 2018
30th IFSCC Congress (International Federation of Societies of Cosmetic Chemists), Munich, 18-21 September, 2018.
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, progressive, and degenerative process 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 various external aggressions and other intrinsic elements. Lipid peroxidation is a consequence of free radicals attack that leads to cell membrane damage. In addition, oxidative stress results in an increase in the glycation process - formation of advanced glycation end products (AGEs), which not only influences the properties of collagen and the extracellular matrix, but also affects the interactions of 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 preventing photodamage caused by UV radiation in human keratinocyte culture. Cells were incubated for 48 hours with three concentrations of the cosmetic formulation previously determined by the MTT method and further exposed to a dose of 10 J/cm² UVA/B radiation. After irradiation, test systems were incubated with fresh culture medium and maintained for 24 hours for the measurement of the receptor for AGE (rAGE) and lipid peroxidation by quantification of malondialdehyde (MDA). As expected, our results demonstrate that UV radiation increases the production of MDA and decreases the amount of free receptor for AGE (rAGEs). However, in comparison to the group only exposed to UV radiation, the cosmetic formulation significantly reduced 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).