{"title":"Coix Seed Extract Prevents Inflammation-mediated Skin Dryness Induced\n by Sodium Dodecyl Sulfate Exposure in HR-1 Hairless Mice","authors":"Feng Li, Yusuke Nakanishi, Kenta Murata, Kanako Shinguchi, Nina Fujita, Shigeki Chiba, Ryuji Takahashi","doi":"10.1055/a-1821-6332","DOIUrl":null,"url":null,"abstract":"Skin inflammation and dryness are the features of surfactant-induced irritant\n contact dermatitis, a common skin disorder. In Japan, Coix seed (CS, Coix\n lacryma-jobi L. var. ma-yuen Stapf) is widely used as a\n traditional medicine and functional supplement to treat skin inflammation and\n dry skin. However, the efficacy of CS against surfactant-induced skin disorders\n has not been reported. Here, we investigated the effect of CS on inflammatory\n dry skin disorders induced by multiple topical applications of sodium dodecyl\n sulfate (SDS), a representative anionic surfactant. Male HR-1 hairless mice\n received a water extract of CS for four weeks. Three weeks after CS\n administration, the dorsal skin of the mice was exposed once daily to\n 10% SDS for five days. CS efficacy was then evaluated by measuring\n epidermal water content; erythema index; severity of skin scaling; epidermal\n thickness; inflammatory cell infiltration; production of pro-inflammatory\n mediators, such as interleukin-1α (IL-1α) and prostaglandin E2\n (PGE2); and protein expression of cyclooxygenase 2 (COX-2), in the dorsal skin.\n Administration of CS markedly attenuated the SDS-induced reduction in epidermal\n water content, elevated erythema index, and severity of skin scaling.\n Histological analysis demonstrated that CS suppressed epidermal hyperplasia and\n macrophage infiltration in SDS-exposed skin. Furthermore, CS significantly\n prevented SDS-induced production of IL-1α and PGE2, as well as COX-2\n upregulation. These results indicate that CS prevents SDS-induced\n inflammation-mediated skin dryness by inhibiting the production of\n pro-inflammatory mediators.","PeriodicalId":199864,"journal":{"name":"Planta Medica International Open","volume":"15 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Planta Medica International Open","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1055/a-1821-6332","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Skin inflammation and dryness are the features of surfactant-induced irritant
contact dermatitis, a common skin disorder. In Japan, Coix seed (CS, Coix
lacryma-jobi L. var. ma-yuen Stapf) is widely used as a
traditional medicine and functional supplement to treat skin inflammation and
dry skin. However, the efficacy of CS against surfactant-induced skin disorders
has not been reported. Here, we investigated the effect of CS on inflammatory
dry skin disorders induced by multiple topical applications of sodium dodecyl
sulfate (SDS), a representative anionic surfactant. Male HR-1 hairless mice
received a water extract of CS for four weeks. Three weeks after CS
administration, the dorsal skin of the mice was exposed once daily to
10% SDS for five days. CS efficacy was then evaluated by measuring
epidermal water content; erythema index; severity of skin scaling; epidermal
thickness; inflammatory cell infiltration; production of pro-inflammatory
mediators, such as interleukin-1α (IL-1α) and prostaglandin E2
(PGE2); and protein expression of cyclooxygenase 2 (COX-2), in the dorsal skin.
Administration of CS markedly attenuated the SDS-induced reduction in epidermal
water content, elevated erythema index, and severity of skin scaling.
Histological analysis demonstrated that CS suppressed epidermal hyperplasia and
macrophage infiltration in SDS-exposed skin. Furthermore, CS significantly
prevented SDS-induced production of IL-1α and PGE2, as well as COX-2
upregulation. These results indicate that CS prevents SDS-induced
inflammation-mediated skin dryness by inhibiting the production of
pro-inflammatory mediators.