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논문 기본 정보

자료유형
학술저널
저자정보
Zhenzhuo Li (Changchun University of Chinese Medicine) Rui Jiang (the Affiliated Hospital to Changchun University of Chinese Medicine) Manying Wang (Changchun University of Chinese Medicine) Lu Zhai (the Affiliated Hospital to Changchun University of Chinese Medicine) Jianzeng Liu (Changchun University of Chinese Medicine) Xiaohao Xu (the Affiliated Hospital to Changchun University of Chinese Medicine) Liwei Sun (the Affiliated Hospital to Changchun University of Chinese Medicine) Daqing Zhao (Changchun University of Chinese Medicine)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.46 No.1
발행연도
2022.1
수록면
115 - 125 (11page)

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초록· 키워드

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Background: Ginsenosides (GS) have potential value as cosmetic additives for prevention of skin photoaging. However, their protective mechanisms against skin barrier damage and their active monomeric constituents are unknown.
Methods: GS monomer types and their relative proportions were identified. A UVB-irradiated BALB/c hairless mouse model was used to assess protective effects of GS components on skin epidermal thickness and transepidermal water loss (TEWL). Skin barrier function, reflected by filaggrin (FLG), involucrin (IVL), claudin-1 (Cldn-1), and aquaporin 3 (AQP3) levels and MAPK phosphorylation patterns, were analyzed in UVB-irradiated hairless mice or HaCaT cells.
Results: Total GS monomeric content detected by UPLC was 85.45% and was largely attributed to 17 main monomers that included Re (16.73%), Rd (13.36%), and Rg1 (13.38%). In hairless mice, GS ameliorated UVB-induced epidermal barrier dysfunction manifesting as increased epidermal thickness, increased TEWL, and decreased stratum corneum water content without weight change. Furthermore, GS treatment of UVB-irradiated mice restored protein expression levels and epidermal tissue distributions of FLG, IVL, Cldn-1, and AQP3, with consistent mRNA and protein expression results obtained in UVB-irradiated HaCaT cells (except for unchanging Cldn-1 expression). Mechanistically, GS inhibited JNK, p38, and ERK phosphorylation in UVB-irradiated HaCaT cells, with a mixture of Rg2, Rg3, Rk3, F2, Rd, and Rb3 providing the same protective MAPK pathway inhibition-associated upregulation of IVL and AQP3 expression as provided by intact GS treatment.
Conclusion: GS protection against UVB-irradiated skin barrier damage depends on activities of six ginsenoside monomeric constituents that inhibit the MAPK signaling pathway.

목차

ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References

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