http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Zhenzhuo Li (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
-
Ginsenosides repair UVB-induced skin barrier damage in BALB/c hairless mice and HaCaT keratinocytes
Zhenzhuo Li,Rui Jiang,Manying Wang,Lu Zhai,Jianzeng Liu,Xiaohao Xu,Liwei Sun,Daqing Zhao 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1
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.
-
Jianzeng Liu,Xiaohao Xu,Jingyuan Zhou,Guang Sun,Zhenzhuo Li,Lu Zhai,Jing Wang,Rui Ma,Daqing Zhao,Rui Jiang,Liwei Sun 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Our previous investigation indicated that the preparation of Panax ginseng Meyer(P. ginseng) inhibited melanogenesis. It comprised salicylic acid (SA), protocatechuic acid (PA), p-coumaricacid (p-CA), vanillic acid (VA), and caffeic acid (CA). In this investigation, the regulatory effects ofP. ginseng phenolic acid monomers on melanin production were assessed. Methods: In vitro and in vivo impact of phenolic acid monomers were assessed. Results: SA, PA, p-CA and VA inhibited tyrosinase (TYR) to reduce melanin production, whereas CA hadthe opposite effects. SA, PA, p-CA and VA significantly downregulated the melanocortin 1 receptor(MC1R), cycle AMP (cAMP), protein kinase A (PKA), cycle AMP-response element-binding protein (CREB),microphthalmia-associated transcription factor (MITF) pathway, reducing mRNA and protein levels ofTYR, tyrosinase-related protein 1 (TYRP1), and TYRP2. Moreover, CA treatment enhanced the cAMP, PKA,and CREB pathways to promote MITF mRNA level and phosphorylation. It also alleviated MITF proteinlevel in a-MSH-stimulated B16F10 cells, comparable to untreated B16F10, increasing the expression ofphosphorylation glycogen synthase kinase 3b (p-GSK3b), b-catenin, p-ERK/ERK, and p-p38/p38. Furthermore, the GSK3b inhibitor promoted p-GSK3b and p-MITF expression, as observed in CA-treatedcells. Moreover, p38 and ERK inhibitors inhibited CA-stimulated p-p38/p38, p-ERK/ERK, and p-MITFincrease, which had negative binding energies with MC1R, as depicted by molecular docking. Conclusion: P. ginseng roots' phenolic acid monomers can safely inhibit melanin production by bidirectionallyregulating melanin synthase transcription. Furthermore, they reduced MITF expression viaMC1R/cAMP/PKA signaling pathway and enhanced MITF post-translational modification via Wnt/mitogen-activated protein kinase signaling pathway.
DBpia
DBpia연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
