Share This Article
Research Frontiers
of Medicinal Plants
DOWNLOAD


下載
人參達瑪烷皂苷Rh2的藥理作用簡述



下載
達瑪烷皂苷Rg1的藥理作用簡述



下載
達瑪烷皂苷Rb1的藥理作用簡述



下載
達瑪烷苷元原人參三醇PPT的藥理作用簡述



下載
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(原人參二醇)誘導非小細胞肺癌細胞凋亡
近年來, 肺癌的發病率和死亡率在世界範圍內呈不斷上升的趨勢,其中80%~85%表現為非小細胞肺癌 ( NSCLC )。 20(S)- 原人參二醇 ( PPD )是從西洋參(Panax quinquefolium L.)莖葉總皂苷中分離、轉化而得到的皂苷元,對非小細胞肺癌 A549細胞具有很強的抑製作用,但其誘導A549細胞發生凋亡以及抑制PI3K/AKT信號轉導通路的作用尚不明確。 本研究採用熒光染色法、瓊脂糖凝膠法、流式細胞法等,檢測了PPD誘導A549細胞凋亡情況;應用Western B...
LANGUAGE 語言選擇

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

© 2015 Yao Hao International Biotechnology Co., Ltd. All Rights Reserved.   Designed by Unique