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


Author: Samara Eberlin

Published at: October 07, 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 an increased glycation process—formation of AGE (advanced glycation end products), which not only influences the properties of collagen and the extracellular matrix but also affects the interactions of cells with the matrix, resulting in physical changes such as migration, growth, proliferation, differentiation, and gene expression. Heat Shock Proteins (HSP) play an important role in the defense mechanism, decreasing the vulnerability of cells to 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-κB, as well as the activity of catalase, superoxide dismutase, and glutathione reductase, using an in vitro model of human fibroblasts and keratinocytes. The active compound decreased the consumption of glutathione reductase, superoxide dismutase, and catalase by 53.3%, 70.1%, and 76.8%, respectively, when compared to the group exposed to UV radiation. We also observed inhibition of DPPH and ABTS radicals at all ECAC concentrations tested. Regarding the synthesis of the inflammatory marker NF-κB, significant reductions were also obtained compared to the only irradiated group. The active compound demonstrated antiglycation activity by decreasing the production of AGEs and HSP-47, as well as increasing receptors for AGEs. The results enable us to infer that ECAC exerts a protective effect against UV radiation through mechanisms involving the capture and neutralization of free radicals, thus sparing the consumption of antioxidant enzymes glutathione reductase, catalase, and superoxide dismutase. A decrease in activation of the HSP-47 chaperone for collagen synthesis protection was also observed, confirming the protective effect of the test substance. Additionally, the compound showed antiglycation activity as it reduced the generation of AGEs induced by 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.