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A novel eye care active complex against UV-induced glycation, inflammation and oxidative stress

A novel eye care active complex against UV-induced glycation, inflammation and oxidative stress
Posted by: Samara Eberlin in 07 de Outubro de 2015

24th EADV (European Academy of Dermatology and Venereology) Congress, Copenhagen, 7-11 October, 2015.
Vanzo ACJR, Pereira AFC, Cascais LC, Mercuri M, Torloni LBO, Lage R, Andrade CC, Yamashita JT, Clerici SP, Eberlin S, Pinheiro ALTA, Pinheiro AS.

Extrinsic aging is attributed to changes in the skin due to lifestyle, being influenced mainly by ultraviolet radiation (UV) but also by pollution resulting from smoking, chemicals, heat and other environmental insults. Solar exposure results in increased glycation process - formation of AGE (advanced glycation end products), which not only influences the properties of collagen and extracellular matrix, but also affects the interactions of cells with the matrix, resulting in changes physical cell such as migration, growth, proliferation, differentiation, and, gene expression. Heat Shock Proteins (HSP) plays an important role in the defense mechanism decreasing the vulnerability of the cell environmental attack, functioning as a chaperone to protect the structure of procollagen during the unfolding phase by binding to a triple-helix. In this study, we evaluated the preclinical effectiveness of an eye care active compound (ECAC) in protecting against photodamage caused by ultraviolet radiation in cultured human fibroblasts and keratinocytes. We measured the synthesis of HSP-47, AGEs, receptor for AGEs (rAGE), NF-?B, as well as the activity of catalase, superoxide dismutase and, glutathione reductase, using an in vitro model of human fibroblast and keratinocytes. The active compound decreased the consumption of glutathione reductase, superoxide dismutase and catalase in 53.3, 70.1 and 76.8%, respectively, when compared to the group submitted to UV radiation. We also observed an inhibition of DPPH and ABTS radical at all ECAC concentrations tested. Regarding the synthesis of inflammatory marker NF-kB, significant reductions were also obtained, compared to only irradiated group. The active compound demonstrated an antiglycation activity by decreasing the production of AGEs and HSP-47, as well as the increase in receptors for AGEs. The results enable us to infer that the ECAC exerts a protective effect against UV radiation by mechanisms that involve the capture and neutralization of free radicals, thus saving the consumption of antioxidant enzymes glutathione reductase, catalase and superoxide dismutase. A decrease in activation of the HSP47 chaperone for collagen synthesis protection was also observed, which confirms the protective effect of the test substance. Additionally, the compound showed an antiglycation activity since it reduced the generation of AGEs-induced UV radiation, as well as increased the amount of unbound receptor for AGE. These findings, associated with the anti-inflammatory effect reported in this study support the use of this active compound in mitigating the harmful effects of prolonged exposure to UV radiation.