Protective effects of Belamcandae Rhizoma against skin damage by ameliorating ultraviolet‐B‐induced apoptosis and collagen degradation in keratinocytes
Ultraviolet‐B light (UV‐B) is a major cause of skin photoaging, inducing cell death and extracellular matrix collapse by generating reactive oxygen species (ROS). Belamcandae Rhizoma (BR), the rhizome of Belamcanda chinensis Leman, exhibits antioxidant properties, but it remains unknown whether BR e...
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Veröffentlicht in: | Environmental toxicology 2019-12, Vol.34 (12), p.1354-1362 |
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Zusammenfassung: | Ultraviolet‐B light (UV‐B) is a major cause of skin photoaging, inducing cell death and extracellular matrix collapse by generating reactive oxygen species (ROS). Belamcandae Rhizoma (BR), the rhizome of Belamcanda chinensis Leman, exhibits antioxidant properties, but it remains unknown whether BR extract ameliorates UV‐B‐induced skin damage. In this study, we evaluated the effects of a standardized BR extract on UV‐B‐induced apoptosis and collagen degradation in HaCaT cells. BR was extracted using four different methods. We used radical‐scavenging assays to compare the antioxidative activities of the four extracts. Cells were irradiated with UV‐B and treated with BR boiled in 70% (vol/vol) ethanol (BBE). We measured cell viability, intracellular ROS levels, the expression levels of antioxidative enzymes, and apoptosis‐related and collagen degradation‐related proteins. The irisflorentin and tectorigenin levels were measured via high‐performance liquid chromatography. BBE exhibited the best radical‐scavenging and cell protective effects of the four BR extracts. BBE inhibited intracellular ROS generation and induced the synthesis of antioxidative enzymes such as catalase and glutathione. BBE attenuated apoptosis by reducing the level of caspase‐3 and increasing the Bcl‐2/Bax ratio. BBE reduced the level of matrix metalloproteinase‐1 and increased that of type I collagen. The irisflorentin and tectorigenin contents were 0.23% and 0.015%, respectively. From these results, BBE ameliorated UV‐B‐induced apoptosis and collagen degradation by enhancing the expression of antioxidative enzymes. It may be a useful treatment for UV‐B‐induced skin damage. |
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ISSN: | 1520-4081 1522-7278 |
DOI: | 10.1002/tox.22836 |