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Abstract
BackgroundOxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. Catechins, which are antioxidants contained in green tea, exert various actions such as anti-inflammatory, anti-bacterial, and anti-cancer actions. In this study, we investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts.MethodsFibroblasts (NIH3T3) under oxidative stress induced by hydrogen peroxide (0.1 mM) were treated with either vehicle or (+)-catechin (0–100 μM). The effect of (+)-catechin on cell viability, apoptosis, phosphorylation of c-Jun terminal kinases (JNK) and p38, and activation of caspase-3 in fibroblasts under oxidative stress were evaluated.ResultsHydrogen peroxide induced apoptotic cell death in fibroblasts, accompanied by induction of phosphorylation of JNK and p38 and activation of caspase-3. Pretreatment of the fibroblasts with (+)-catechin inhibited hydrogen peroxide-induced apoptosis and reduced phosphorylation of JNK and p38 and activation of caspase-3.Conclusion(+)-Catechin protects against oxidative stress-induced cell death in fibroblasts, possibly by inhibiting phosphorylation of p38 and JNK. These results suggest that (+)-catechin has potential as a therapeutic agent for the prevention of skin aging.
Highlights
Oxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin
(+)-Catechin inhibits oxidative stress-induced apoptosis in fibroblasts To determine whether (+)-catechin has an inhibitory effect on oxidative stress-induced apoptosis in fibroblasts, we assessed the apoptosis of fibroblasts in either the presence or absence of (+)-catechin by Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. (+)-Catechin (10 μM)-treated fibroblasts showed significant decreases in the percentage of cells positive for TUNEL staining, compared to vehicle-treated cells (9.14% ± 0.6% vs. 1.86% ± 0.3%; Figure 4)
Effect of catechin on the activation of caspase-3 by H2O2-induced oxidative stress in fibroblasts Western blotting analysis using an anti-cleaved caspase-3 antibody showed that the level of cleaved caspase-3 induced by H2O2 was reduced by treatment with 10 μM (+)-catechin (Figure 5). These results suggest that (+)-catechin inhibits caspase-3-dependent apoptosis induced by oxidative stress in fibroblasts
Summary
Oxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. We investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts. Skin wrinkles and sagging are important factors defining skin youthfulness. Development of methods to reduce skin wrinkles and prevent sagging skin has become an important research topic in aesthetic and anti-aging medicine. Fibroblasts play a key role in the production of these extracellular matrix components in the skin. Skin aging is the consequence of reduced numbers of fibroblasts, lower levels of extracellular matrix proteins, and decreased skin elasticity and tonus, thereby resulting in the formation of wrinkles [2].
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