8-Prenylkaempferol Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

354.4

<1mg/ml refers to the product slightly soluble or insoluble

C20H18O6

CC(C)=CCc(c(OC(c(cc1)ccc1O)=C1O)c(c(O)c2)C1=O)c2O

28610-31-3

p38
NF-kappaB
PI3K

MC3T3-E1 cells were exposed to 8-Prenylkaempferol and the cytotoxicity was assayed. Osteoblast differentiation and maturation were evaluated by analyzing alkaline phosphatase (ALP) activity and cell mineralization, respectively. RT-PCR and Western blot were executed to determine the effects of 8-Prenylkaempferol on osteoblast differentiation-related gene expression and signaling pathway. 8-Prenylkaempferol significantly promoted ALP activity, up-regulated mRNA expressions of osteocalcin, osteopontin, and type I collagen, and induced bone nodules formation. Induction of differentiation by 8-Prenylkaempferol was associated with increased bone morphogenetic protein (BMP)-2 expression, and sequentially up-regulated the phosphorylations of Smad1/5/8 and p38, and increased the nuclear translocation of runt-related transcription factor 2 (Runx2). Addition of BMP-2 antagonist noggin blocked 8-Prenylkaempferol and recombinant mouse BMP-2-induced ALP activity, reconfirming that BMP-2 production is required in 8-Prenylkaempferol-mediated osteoblast differentiation. Noggin also abrogated 8-Prenylkaempferol evoked phosphorylations of Smad1/5/8 and p38, suggesting that BMP-2 signaling is required for p38 activation in 8-Prenylkaempferol-treated cells. Application of p38 inhibitor SB203580 repressed not only 8-Prenylkaempferol-mediated activation of ALP, but also the nuclear translocation of Runx2 and bone nodules formation[1]

MAPK; p38 MAPK; NF-kappab; PI3K/Akt/mTOR signaling