Buddlejasaponin IV Inhibitor

Solid. Powder

98.00%

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

943.12

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

C48H78O18

C[C@@H]1[C@@H]([C@@H]([C@H]([C@@H](O1)O[C@H]2CC[C@]3([C@H]([C@]2(C)CO)CC[C@@]4([C@@H]3C=C[C@@]56[C@]4(C[C@@H]([C@@]7([C@H]5CC(CC7)(C)C)CO6)O)C)C)C)O[C@H]8[C@@H]([C@H]([C@@H]([C@H](O8)CO)O)O)O)O[C@H]9[C@@H]([C@H]([C@@H]([C@H](O9)CO)O)O)O)O

139523-30-1

Chk
Akt
PARP

The study investigated whether Buddlejasaponin IV could prevent oral carcinogenesis by inhibiting the growth of immortalized human oral keratinocytes (IHOKs). Buddlejasaponin IV reduced cell viability and induced cell cycle arrest at G2/M phase and apoptotic morphological changes in IHOKs. Buddlejasaponin IV inhibited the levels of cyclin B1, Cdc2 and Cdc25C, but enhanced Chk2 phosphorylation. The increased levels of pRb and p21 protein and the activation of p53 were also noted in Buddlejasaponin IV-treated IHOKs. In addition, Buddlejasaponin IV induced cytochrome c release from mitochondria by reducing antiapoptotic Bcl-2 levels and increasing pro-apoptotic Bax levels. Buddlejasaponin IV treatment,resulted in the activation of caspase-9 and caspase-3. PARP cleavage was also clearly observed in the Buddlejasaponin IV-treated IHOKs. Furthermore, the expression of the Fas death receptor and Fas ligand was induced and procaspase-8 level was suppressed by Buddlejasaponin IV treatment, Taken together, Buddlejasaponin IV treatment,inhibited the growth of IHOK cells via the induction of p53-dependent cell cycle arrest at the G2/M phase and apoptosis via both mitochondrial-dependent and death receptor-mediated pathways[1]

Cell Cycle/Checkpoint; Chk; Cytoskeletal Signaling; Chromatin/Epigenetic