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達瑪烷苷元原人參二醇PPD的藥理作用簡述


 

達瑪烷苷元PPD抑制紫外線誘導的MMP表達

達瑪烷苷元PPD誘導神經膠質瘤細胞凋亡(死亡)
20S –原人參二醇(達瑪烷苷元PPD)是一些人參皂甙的代謝衍生物。 在本研究中,達瑪烷苷元PPD能夠誘導人神經膠質瘤細胞(SF188和U87MG)產生程序性細胞死亡(凋亡)。對於的SF188細胞的,PPD激活了多種凋亡酶(如PPD在3小時內激活了凋亡酶3、8、7、9,並快速誘導細胞凋亡)。這種作用能夠內凋亡酶抑製劑和抗氧化劑阻斷,進一步說明PPD是通過激活凋亡酶來誘導腫瘤細胞凋亡。 化合物PPD雖然誘導U87MG腫瘤細胞凋亡,但PPD沒有激活任何凋亡酶。進一步研究發現,PPD是通過抑制細胞...
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MMP-1 is an enzyme which is able to digest collagen in the skin, and overe-exposure to UV will excessively activate MMP-1, thus leads to collagen loss in the skin, acceleartes the skin aging process. New findings in this article suggest dammarane sapogenin PPD could help the skin resist against UV abuse and retard skin aging.

Related Articles
20-O-β-d-Glucopyranosyl-20(S)-Protopanaxadiol Suppresses UV-Induced MMP-1 Expression Through AMPK-Mediated mTOR Inhibition as a Downstream of the PKA-LKB1 Pathway.
J Cell Biochem. 2014 May 12;
Authors: Shin DJ, Kim JE, Lim TG, Jeong EH, Park G, Kang NJ, Park JS, Yeom MH, Oh DK, Bode AM, Dong Z, Lee HJ, Lee KW

Abstract
Various health effects have been attributed to the ginsenoside metabolite 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol (GPD); however, its effect on ultraviolet (UV)-induced matrix metalloproteinase (MMP)-1 expression and the mechanism underlying this effect are unknown.
We examined the inhibitory effect of GPD on UV-induced MMP-1 expression and its mechanisms in human dermal fibroblasts (HDFs).
GPD attenuated UV-induced MMP-1 expression in HDFs and suppressed the UV-induced phosphorylation of mammalian target of rapamycin (mTOR) and p70(S6K) without inhibiting the activity of phosphatidylinositol 3-kinase and Akt, which are well-known upstream kinases of mTOR.
GPD augmented the phosphorylation of liver kinase B1 (LKB1) and adenosine monophosphate-activated protein kinase (AMPK), which are inhibitors of mTOR, to a greater extent than UV treatment alone.
Similar to GPD, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranosyl 5′-monophosphate (AICAR), an activator of AMPK, augmented UV-induced AMPK phosphorylation to a greater extent than UV treatment alone, resulting in the inhibition of MMP-1 expression. AICAR also decreased the phosphorylation of mTOR and p70(S6K) .
However, compound C, an antagonist of AMPK, increased MMP-1 expression. In HDF cells with AMPK knock-down using shRNA, MMP-1 expression was increased.
These results indicate that AMPK activation plays a key role in MMP-1 suppression. Additionally, the cAMP-dependent protein kinase (PKA) inhibitor, H-89, antagonized GPD-mediated MMP-1 suppression via the inhibition of LKB1.
Our results suggest that the suppressive activity of GPD on UV-induced MMP-1 expression is due to the activation of AMPK as a downstream of the PKA-LKB1 pathway.
J. Cell. Biochem. © 2014 Wiley Periodicals, Inc.
PMID: 24821673 [PubMed - as supplied by publisher]

Source: PPT and PPD

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