Clinical and experimental dermatology · 2016
Potent effects of peracetylated (-)-epigallocatechin-3-gallate against hydrogen peroxide-induced damage in human epidermal melanocytes via attenuation of oxidative stress and apoptosis.
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Ning W, Wang S, Liu D, Fu L, Jin R, Xu A
Аннотация
BACKGROUND: Damage to melanocytes induced by oxidative stress plays an important role in the pathogenesis of vitiligo. A polyphenol found in green tea, (-)-epigallocatechin-3-gallate (EGCG), exhibits certain antioxidative effects in the treatment of various diseases. The major problem that limits the clinical application of this polyphenol is its low bioavailability and stability. Peracetylated EGCG (AcEGCG), a fully acetylated derivative of EGCG, is more stable and bioavailable than EGCG, but the effects of its action on human epidermal melanocytes have not been elucidated.
AIM: To compare the protective effects of AcEGCG and EGCG on hydrogen peroxide (H2 O2 )-induced damage to human melanocytes.
METHODS: Effects of AcEGCG and EGCG on human melanocytes were examined by measuring cell viability, levels of reactive oxygen species (ROS), the mitochondrial membrane potential (ΔΨm)and protein levels of caspase-9, caspase-3 and p38 mitogen-activated protein kinase.
RESULTS: Both AcEGCG and EGCG decreased ROS generation, restored lost mitochondrial membrane potential and reduced H2 O2 -induced apoptosis in melanocytes. All of these effects were more pronounced with AcEGCG than with EGCG. Furthermore, AcEGCG effectively suppressed H2 O2 -induced p38 mitogen-activated protein kinase phosphorylation, which has been suggested to contribute to melanocyte damage.
CONCLUSIONS: AcEGCG is a more potent agent than EGCG for protection of melanocytes from oxidative damage.
AIM: To compare the protective effects of AcEGCG and EGCG on hydrogen peroxide (H2 O2 )-induced damage to human melanocytes.
METHODS: Effects of AcEGCG and EGCG on human melanocytes were examined by measuring cell viability, levels of reactive oxygen species (ROS), the mitochondrial membrane potential (ΔΨm)and protein levels of caspase-9, caspase-3 and p38 mitogen-activated protein kinase.
RESULTS: Both AcEGCG and EGCG decreased ROS generation, restored lost mitochondrial membrane potential and reduced H2 O2 -induced apoptosis in melanocytes. All of these effects were more pronounced with AcEGCG than with EGCG. Furthermore, AcEGCG effectively suppressed H2 O2 -induced p38 mitogen-activated protein kinase phosphorylation, which has been suggested to contribute to melanocyte damage.
CONCLUSIONS: AcEGCG is a more potent agent than EGCG for protection of melanocytes from oxidative damage.