BuddlejasaponinIV CAS NO.139523-30-1

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Chemical Properties of Buddlejasaponin IV

Source of Buddlejasaponin IV

The herbs of Buddleja lindleyana Fort.

Biological Activity of Buddlejasaponin IV

Preparing Stock Solutions of Buddlejasaponin IV

References on Buddlejasaponin IV

Buddlejasaponin IV induces cell cycle arrest at G2/M phase and apoptosis in immortalized human oral keratinocytes.[Pubmed:21394802]

Phytother Res. 2011 Oct;25(10):1503-10.

Buddlejasaponin IV (BS-IV), a major component of Pleurospermum kamtschaticum, exerts antiinflammatory and cytotoxic effects against cancer cells. The study investigated whether BS-IV could prevent oral carcinogenesis by inhibiting the growth of immortalized human oral keratinocytes (IHOKs). BS-IV reduced cell viability and induced cell cycle arrest at G2/M phase and apoptotic morphological changes in IHOKs. BS-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 BS-IV-treated IHOKs. In addition, BS-IV induced cytochrome c release from mitochondria by reducing antiapoptotic Bcl-2 levels and increasing pro-apoptotic Bax levels. BS-IV treatment resulted in the activation of caspase-9 and caspase-3. PARP cleavage was also clearly observed in the BS-IV-treated IHOKs. Furthermore, the expression of the Fas death receptor and Fas ligand was induced and procaspase-8 level was suppressed by BS-IV treatment. Taken together, BS-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. Thus, BS-IV can be considered an excellent candidate for a chemopreventive agent to block the progression of HPV-induced oral carcinogenesis.

The Inhibitory Effect of Buddlejasaponin IV on the Growth of YD-10B Human Oral Squamous Cell Carcinoma Cells.[Pubmed:25337562]

J Cancer Prev. 2013 Dec;18(4):330-6.

BACKGROUND: Buddlejasaponin IV (BS-IV), a triterpene saponin isolated from Pleurospermum kamtschaticum HOFFMANN (Umbelliferae), is known to have potent anti-inflammatory activity and cytotoxicity against diverse cancer cell lines. In the present study, we attempted to verify whether BS-IV could inhibit cell growth, and induce cell cycle arrest and apoptosis in highly invasive YD-10B human oral squamous cell carcinoma (OSCC) cells. METHODS: YD-10B cells were treated with various concentrations of BS-IV, and the cell viability was evaluated by MTT assay. Flow cytometry was conducted to examine cell phase distribution and DAPI staining was performed to observe apoptotic morphological changes in BS-IV-treated YD-10B cells. Western blot analysis was used to investigate the expression of proteins associated with cell cycle arrest and apoptosis. RESULTS: BS-IV treatment significantly reduced the viability of YD-10B cells and partially arrested cell cycle progression at the G2/M phase. Treatment with BS-IV substantially decreased the levels of cyclin B1 and stimulated the phosphorylation of checkpoint kinase 2 (Chk2). The expression of p21 was increased but the phosphorylation of Akt was inhibited in BS-IV-treated YD-10B cells. Furthermore, BS-IV induced release of cytochrome c from mitochondria by reducing anti-apoptotic Bcl-2 level and increasing pro-apoptotic Bax level. Active caspase-3 level and the cleavage of poly (ADP-ribose) polymerase (PARP) were enhanced by BS-IV treatment. In addition, BS-IV increased the expression of Fas death receptor and its ligand (FasL) in YD-10B cells. CONCLUSIONS: The treatment with BS-IV inhibits the growth of YD-10B cells by inducing p21-dependent cell cycle arrest at G2/M phase and apoptosis through both mitochondrial-dependent and death receptor-mediated pathways. Thus, BS-IV is an excellent candidate for a chemopreventive agent to block the progression of human OSCC.

The MeOH extract of Pleurospermum kamtschaticum and its active component buddlejasaponin (IV) inhibits intrinsic and extrinsic hyperlipidemia and hypercholesterolemia in the rat.[Pubmed:17433587]

J Ethnopharmacol. 2007 Jun 13;112(2):255-61.

The inhibitory effect of the MeOH extract of Pleurospermum kamtschaticum (Umbelliferase) and its fractions were tested in hyperlipidemic and hypercholesterolemic rats using four animal models induced using poloxamer-407 or using Triton WR-1339 as intrinsic inducers and by 30% corn oil or high cholesterol diet as extrinsic inducers. We measured serum triglyceride, total cholesterol, HDL-cholesterol and LDL-cholesterol levels as measures of its hypocholesterolemic or hypolipidemic effects. Since the MeOH extract and the BuOH fraction of Pleurospermum kamtschaticum were found to be active using these four hypolipidemic assays, its major saponin Buddlejasaponin IV {BS(IV)} isolated from the BuOH fraction were also tested to demonstrate the active components. BS(IV) was found to significantly inhibit hypercholesterolemia and hyperlipidemia by extrinsic and intrinsic inducers. In particular, BS(IV) reduced the blood thiobarbituric acid reactive substance (TBARS) and hydroxy radical levels, and increased superoxide dismutase activity in high cholesterol diet-induced rats, thus suggesting that BS(IV) reduces oxidative stress caused by a high cholesterol diet. Moreover, these effects of BS(IV) were comparable to probucol, which was used as a positive control. These results suggested that Pleurospermum kamtschaticum which is traditionally used to treat atherosclerosis and its active major saponin BS(IV) could be used to treat hypercholesterolemia or hyperlipidemia.

Anti-inflammatory effect of buddlejasaponin IV through the inhibition of iNOS and COX-2 expression in RAW 264.7 macrophages via the NF-kappaB inactivation.[Pubmed:16520738]

Br J Pharmacol. 2006 May;148(2):216-25.

Buddlejasaponin IV isolated from Pleurospermum kamtschatidum is an anti-inflammatory compound that inhibits NO, PGE(2) and TNF-alpha production. Here, we studied the mode of action of this compound. Buddlejasaponin IV (2.5-10 microM) reduced lipopolysaccaride (LPS (1 microg ml(-1)))-induced levels of iNOS and COX-2 at the protein levels, and iNOS, COX-2, TNF-alpha, interleukin (IL)-1beta and IL-6 mRNA expression in RAW 264.7 macrophages in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. Buddlejasaponin IV inhibited the LPS-induced activation of nuclear factor-kappaB (NF-kappaB), a transcription factor necessary for proinflammatory mediators, iNOS, COX-2, TNF-alpha, IL-1beta and IL-6 expression. This effect was accompanied by a parallel reduction in IkappaB-alpha degradation and phosphorylation, and by the nuclear translocation of the NF-kappaB p65 subunit. The effects of Buddlejasaponin IV on acute phase inflammation were studied on serotonin- and carrageenan-induced paw edema. The antiedematous effect of Buddlejasaponin IV was compared with 10 mg kg(-1) of indomethacin p.o. Maximum inhibitions of 26 and 41% were noted at a dose of 20 mg kg(-1) for serotonin- and carrageenan-induced paw edema, respectively. The analgesic effect of Buddlejasaponin IV was evaluated using acetic acid-induced writhing and hot-plate tests. Buddlejasaponin IV (10 and 20 mg kg(-1), p.o.) was found to have a marked analgesic effect in both models. These results suggest that the inhibitions of the expressions of iNOS, COX-2, TNF-alpha, IL-1beta and IL-6 by blocking NF-kappaB activation, are responsible for the anti-inflammatory effects of Buddlejasaponin IV isolated from P. kamtschatidum.

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