Search

A new resveratrol oligomer (1) together with eight related components (2- 9) were isolated from the seed extract of Paeonia lactiflora (Paeoniaceae) as active principles responsible for the inhibition of beta-site APP-cleaving enzyme 1 (BACE-1) in vitro. The chemical structure of 1 was established as (-)-7a,8a- CIS- ε-viniferin with the aid of spectroscopic analyses including NOESY experiments. All isolated resveratrol oligomers (1- 9) demonstrated significant inhibition on baculovirus-expressed BACE-1 in a dose-dependent manner, which was assessed by the FRET assay using Rh-EVNLDAEFK as a substrate in vitro.

Three new guaiane-type sesquiterpene lactones (1-3), together with nine related sesquiterpenes (4-12), were isolated from the whole extract of Ixeris dentata (Asteraceae). The chemical structures of isolates 1-12 were established by spectroscopic analyses as 3 β,8 β-dihydroxy-guaia-10(14)-en-1 α,4 α,5 α,6 β,7 α,11 βH-12,6 α-olide (1), ixerin N 6'- O-acetate (2), ixerisoside A 6'- O-acetate (3), ixerin N ( 4), ixerisoside A (5), ixerin M (6), tectroside (7), 8-epidesacylcynaropicrin glucoside (8), 8-epiisolipidiol (9), 11 βH-11,13-dihydrointegrifolin (10) 8 β-hydroxy-4 β,15-dihydrozaluzanin C (11), and integrifolin (12). Compounds 1-12 were evaluated for their inhibitory effect on the proliferation of the cultured human tumor cell lines MES-SA, MES-SA/DX5, HCT-15, and HCT15/CL02 in vitro.

Farnesylation of the activated RAS oncogene product by protein farnesyltransferase (FTase) is a critical step for its oncogenic function. Bioassay-guided purification of Ferula asafoetida (Umbelliferae) extract led to the isolation of the coumarin-derived sesquiterpene galbanic acid (1) as an active principal for FTase inhibitory activity, together with the four structurally related sesquiterpenes karatavicinol (2), umbelliprenin (3), farnesiferol B (4), and farnesiferol C (5). The 50 % inhibitory concentration (IC (50)) of 1 against FTase in an enzyme-based assay was calculated as 2.5 µM. Compound 1 also demonstrated potent inhibition of the proliferation of oncogenic RAS-transformed NIH3T3/Hras-F in a dose-dependent manner. The IC (50) value of 1 on the proliferation of oncogenic RAS-transformed NIH3T3/Hras-F cells was calculated as 16.2 µM, whereas its IC (50) value on control vector-transfected normal RAS-containing NIH3T3/ZIPneo cells was 58.5 µM.