Skin pharmacology and physiology · 2026
Novel Glyceryl Ascorbate Derivatives Inhibit Type 2 Alarmin Cytokine Induction and Promote Expression of Epidermal Barrier Function-Related Factors in Human Keratinocytes in vitro.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sahara Shunya, Wakita Natsuki, Iwai Miki, Ueno Ayumi, Kuribayashi Miki, Nakaoji Koich, Hamada Kazuhiko, Fujimoto Manabu
Аннотация
INTRODUCTION: Atopic dermatitis is characterized by the interplay among type 2 immune responses, skin barrier dysfunction, and pruritus. Despite the pivotal role of interleukin-33 in the pathogenesis of the disease, novel therapeutic strategies remain limited.
METHODS: In this study, we investigated the effects of 2-O-glyceryl-6-O-hexadecanoyl ascorbic acid (2GA16), assessing its impact on inflammatory cytokine production in an epidermal cell-based atopic dermatitis model. Specifically, 2GA16 was introduced to cultured keratinocytes in an inflammatory state induced by phorbol-12-myristate-13-acetate. The inhibitory effects on inflammatory cytokines were confirmed through gene expression analysis.
RESULTS: The analysis revealed that 2GA16 suppressed the increased expression levels of alarmins, particularly interleukin-33, in a dose-dependent manner (p < 0.01). Epidermal cells treated with 2GA16 exhibited increased expression levels of filaggrin and involucrin, both crucial to epidermal barrier formation (p < 0.05). Such changes were further supported by Western blot analysis and ex vivo tissue staining, which qualitatively showed corresponding changes at the protein level.
CONCLUSION: These findings suggest that 2GA16 may mitigate the symptoms of atopic dermatitis by inhibiting the induction of type 2 alarmin cytokines in keratinocytes and restoring their capacity to form effective epidermal barriers.
METHODS: In this study, we investigated the effects of 2-O-glyceryl-6-O-hexadecanoyl ascorbic acid (2GA16), assessing its impact on inflammatory cytokine production in an epidermal cell-based atopic dermatitis model. Specifically, 2GA16 was introduced to cultured keratinocytes in an inflammatory state induced by phorbol-12-myristate-13-acetate. The inhibitory effects on inflammatory cytokines were confirmed through gene expression analysis.
RESULTS: The analysis revealed that 2GA16 suppressed the increased expression levels of alarmins, particularly interleukin-33, in a dose-dependent manner (p < 0.01). Epidermal cells treated with 2GA16 exhibited increased expression levels of filaggrin and involucrin, both crucial to epidermal barrier formation (p < 0.05). Such changes were further supported by Western blot analysis and ex vivo tissue staining, which qualitatively showed corresponding changes at the protein level.
CONCLUSION: These findings suggest that 2GA16 may mitigate the symptoms of atopic dermatitis by inhibiting the induction of type 2 alarmin cytokines in keratinocytes and restoring their capacity to form effective epidermal barriers.