Abstract

Ultraviolet (UV) light, a major risk factor for external skin photoaging, induces oxidative stress in skin. UV causes a breakdown of skin homeostasis by impairing the extracellular matrix and inducing cell death. Tectorigenin, a constituent of leopard lily (Belamcanda chinensis L.) rhizome, has been reported to possess antioxidant, hair-darkening, and anti-inflammatory activities; however, the effect of tectorigenin on UV-B-induced skin damage is unknown. Here, we investigated the anti-skin-damage effects of tectorigenin against UV-B-stimulated oxidative stress in human keratinocytes. We irradiated HaCaT cells with UV-B (25 mJ/cm2), followed by treatment with tectorigenin for 24 h. We found that tectorigenin decreased the levels of intracellular reactive oxygen species by increasing the expression of anti-oxidative enzymes, such as glutathione and catalase. Furthermore, tectorigenin inhibited apoptosis by reducing caspase-3- and Bcl-2-associated protein-X levels, and increasing Bcl-2 protein levels. Tectorigenin also decreased matrix metalloproteinase-1 levels and increased type 1 collagen levels, thus preventing collagen degradation. These data demonstrate that tectorigenin exerts anti-skin-damage effects in human keratinocytes by attenuating UV-B-induced hyper-oxidation, apoptosis, and collagen degradation.

Highlights

  • Physiological aging of the skin includes the formation of wrinkles, pigmentation, and drying.Two types of skin aging are recognized: intrinsic aging, a natural phenomenon that occurs as humans age, and external aging, which is caused by exposure to the external environment [1]

  • This study investigated the effects of tectorigenin on UV-B-induced keratinocyte apoptosis and collagen degradation

  • We showed that tectorigenin inhibits UV-B-induced cell death and intracellular reactive oxygen species (ROS) generation in keratinocytes

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Summary

Introduction

Physiological aging of the skin includes the formation of wrinkles, pigmentation, and drying. Two types of skin aging are recognized: intrinsic aging, a natural phenomenon that occurs as humans age, and external aging, which is caused by exposure to the external environment [1]. External aging is mediated by external factors, such as solar ultraviolet-A (UV-A), UV-B, and air pollution. They generate reactive oxygen species (ROS) in the skin [2]. UV-A, a long wavelength of ultraviolet (315–400 nm), is known to penetrate into skin more deeply than UV-B and damages the dermis. UV-B, a medium wavelength of ultraviolet (280–315 nm), damages epidermis by causing direct DNA damage [3]

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