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Antimelanogenesis and skin-protective activities of Panax ginseng calyx ethanol extract

BACKGROUND: The antioxidant effects of Panax ginseng have been reported in several articles; however, little is known about the antimelanogenesis effect, skin-protective effect, and cellular mechanism of Panax ginseng, especially of P. ginseng calyx. To understand how an ethanol extract of P. ginsen...

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Detalles Bibliográficos
Autores principales: Lee, Jeong-Ook, Kim, Eunji, Kim, Ji Hye, Hong, Yo Han, Kim, Han Gyung, Jeong, Deok, Kim, Juewon, Kim, Su Hwan, Park, Chanwoong, Seo, Dae Bang, Son, Young-Jin, Han, Sang Yun, Cho, Jae Youl
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026384/
https://www.ncbi.nlm.nih.gov/pubmed/29983620
http://dx.doi.org/10.1016/j.jgr.2018.02.007
Descripción
Sumario:BACKGROUND: The antioxidant effects of Panax ginseng have been reported in several articles; however, little is known about the antimelanogenesis effect, skin-protective effect, and cellular mechanism of Panax ginseng, especially of P. ginseng calyx. To understand how an ethanol extract of P. ginseng berry calyx (Pg-C-EE) exerts skin-protective effects, we studied its activities in activated melanocytes and reactive oxygen species (ROS)–induced keratinocytes. METHODS: To confirm the antimelanogenesis effect of Pg-C-EE, we analyzed melanin synthesis and secretion and messenger RNA and protein expression levels of related genes. Ultraviolet B (UVB) and hydrogen peroxide (H(2)O(2)) were used to induce cell damage by ROS generation. To examine whether this damage is inhibited by Pg-C-EE, we performed cell viability assays and gene expression and transcriptional activation analyses. RESULTS: Pg-C-EE inhibited melanin synthesis and secretion by blocking activator protein 1 regulatory enzymes such as p38, extracellular signal-regulated kinases (ERKs), and cyclic adenosine monophosphate response element–binding protein. Pg-C-EE also suppressed ROS generation induced by H(2)O(2) and UVB. Treatment with Pg-C-EE decreased the expression of matrix metalloproteinases, mitogen-activated protein kinases, and hyaluronidases and increased the cell survival rate. CONCLUSION: These results suggest that Pg-C-EE may have antimelanogenesis properties and skin-protective properties through regulation of activator protein 1 and cyclic adenosine monophosphate response element–binding protein signaling. Pg-C-EE may be used as a skin-improving agent, with moisture retention and whitening effects.