薏苡仁提取物可预防十二烷基硫酸钠暴露致HR-1无毛小鼠炎症介导的皮肤干燥

Feng Li, Yusuke Nakanishi, Kenta Murata, Kanako Shinguchi, Nina Fujita, Shigeki Chiba, Ryuji Takahashi
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引用次数: 1

摘要

皮肤炎症和干燥是表面活性剂引起的刺激性接触性皮炎的特征,这是一种常见的皮肤疾病。在日本,薏苡仁(CS, Coix lacryma-jobi L. var. ma-yuen Stapf)被广泛用作治疗皮肤炎症和皮肤干燥的传统药物和功能性补充剂。然而,CS对表面活性剂引起的皮肤疾病的疗效尚未见报道。在这里,我们研究了CS对多次局部应用十二烷基硫酸钠(SDS)引起的炎症性干性皮肤疾病的影响,SDS是一种典型的阴离子表面活性剂。雄性HR-1无毛小鼠连续4周给予水提物。CS给药3周后,将小鼠背部皮肤每天1次暴露于10% SDS,连续5天。然后通过测定表皮含水量来评价CS的疗效;红斑指数;皮肤脱落的严重程度;表皮厚度;炎性细胞浸润;促炎介质的产生,如白细胞介素-1α (IL-1α)和前列腺素E2 (PGE2);和背侧皮肤环氧化酶2 (COX-2)的蛋白表达。CS可显著减轻sds诱导的表皮含水量减少、红斑指数升高和皮肤脱屑的严重程度。组织学分析表明,CS抑制了sds暴露皮肤的表皮增生和巨噬细胞浸润。此外,CS显著阻止sds诱导的IL-1α和PGE2的产生,以及COX-2的上调。这些结果表明,CS通过抑制促炎介质的产生来预防sds诱导的炎症介导的皮肤干燥。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coix Seed Extract Prevents Inflammation-mediated Skin Dryness Induced by Sodium Dodecyl Sulfate Exposure in HR-1 Hairless Mice
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.
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