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Inhibitory effects of curcuminoids from Curcuma longa on matrix metalloproteinase-1 expression in keratinocytes and fibroblasts
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  • Inhibitory effects of curcuminoids from Curcuma longa on matrix metalloproteinase-1 expression in keratinocytes and fibroblasts
  • Inhibitory effects of curcuminoids from Curcuma longa on matrix metalloproteinase-1 expression in keratinocytes and fibroblasts
저자명
Jang. Se-Hyun,Chun. Jae-Moo,Shin. Eun-Myoung,Kim. Ho-Jeoung,Kim. Yeong-Shik
간행물명
Journal of pharmaceutical investigation
권/호정보
2012년|42권 1호|pp.33-39 (7 pages)
발행정보
한국약제학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Because aging and inflammation mechanisms share common signaling pathways and mediators, natural products with anti-inflammatory effects are also good candidates as anti-aging agents. Bismethoxycurcumin, demethoxycurcumin, and curcumin are three curcuminoids that can be isolated from Curcuma longa and are well known for their anti-inflammatory and anti-cancer activities. In this study, we examined the anti-wrinkle effects of three curcuminoids from Curcuma longa in keratinocytes and fibroblasts to determine whether an anti-inflammatory agent could also be developed as an anti-aging treatment. The inhibitory effects of UV-B-induced upregulation of nuclear factor-kappaB (NF-${kappa}B$) activity were detected by a reporter gene assay. Tumor necrosis factor (TNF-${alpha}$) release was detected by reverse transcriptase-polymer chain reaction (RT-PCR), and matrix metalloprotease-1 (MMP-1) expression was determined by western blot and enzymelinked immunosorbent assay (ELISA). UV-B induced TNF-${alpha}$ release through NF-${kappa}B$ activation in keratinocytes. Three curcuminoids inhibited the UV-B-induced TNF-${alpha}$ mRNA expression. Specifically, demethoxycurcumin and bisdemethoxycurcunim inhibited UV-B-induced NF-${kappa}B$ activation in HaCaT keratinocytes and reduced the expression of MMP-1 in both keratinocytes and fibroblasts. We found that curcuminoids have anti-wrinkle activity through the inhibition of UV-B induction in keratinocytes and TNF-${alpha}$ induction in fibroblasts. Our results suggest that wrinkle formation and inflammation have common signaling pathways.