Ardisiacrispin A
Ardisiacrispin A has cytotoxic activity toward HepG2 cancer cell with the GI(50) value of 1.56μM, it could inhibit the proliferation of Bel-7402 cells by inducing apoptosis and disassembling microtubule.Ardisiacrispin(A+B) exhibit prominent abilities to inhibit the proliferation of HL-60 cells by blocking the cell cycle at S phase and inducing apoptosis.
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J Asian Nat Prod Res. 2008 Jul-Aug;10(7-8):739-46.
Pro-apoptotic and microtubule-disassembly effects of ardisiacrispin (A+B), triterpenoid saponins from Ardisia crenata on human hepatoma Bel-7402 cells.[Pubmed:
18696326]
Ardisiacrispin A+Ardisiacrispin B is a mixture of Ardisiacrispin A and ardisiacrispin B, derived from Ardisia crenata with a fixed proportion (2:1).
METHODS AND RESULTS:
The present study was conducted to investigate its anticancer activity on human cancer cells and its underlying mechanism of action. The (IC50)s of Ardisiacrispin A+Ardisiacrispin B on proliferation of several human cancer cell lines were in the range of 0.9-6.5 microg/ml by sulphorhodamine B-based colorimetric assay, in which Bel-7402 was the most sensitive cell line. Moreover, Ardisiacrispin A+Ardisiacrispin B induced dose-dependent apoptosis in Bel-7402 cells at doses of 1-10 microg/ml by flow cytometry, and resulted in the changes of the mitochondrial membrane depolarization, membrane permeability enhancement, and nuclear condensation in a dose-dependent manner through high-content screening analysis. Furthermore, Ardisiacrispin A+Ardisiacrispin B could disassemble microtubule in Bel-7402 cells; the fluorescence intensity of microtubules decreased at the concentration of 5-20 microg/ml.
CONCLUSIONS:
These findings suggest that Ardisiacrispin A+Ardisiacrispin B could inhibit the proliferation of Bel-7402 cells by inducing apoptosis and disassembling microtubule.
Chin. Pharm. Bull., 2007, 23(5):585-90.
Study on inhibitory effects and mechanism of ardisiacrispin (A + B) on human promyeloleukemic HL-60 cells[Reference:
WebLink]
To study the inhibitory effect of Ardisiacrispin A+Ardisiacrispin B on human promyeloleukemic HL-60 cells and the underlying mechanism.
METHODS AND RESULTS:
Cell growth inhibition in vitro was evaluated with MTT assay. Ardisiacrispin A+Ardisiacrispin B -induced cell cycle block and apoptosis were investigated using flow cytometry assay. Apoptitic bodies were detected by PI staining. Western blot was applied to determine modification of certain protein related to apoptosis. Ardisiacrispin A+Ardisiacrispin B displayed dose dependent growth inhibition ability on HL-60 cells with the IC50 value of 4.2 mg·L-1 for 48 h. Ardisiacrispin A+Ardisiacrispin B dose-dependently arrested HL-60 cells at the S phase of the cell cycle in the range of 1.0 - 5.0 mg·L-1, cells at S phase in treated group was 1.26inverted commas 1.46 and 1.71 times of control group for 6inverted commas24 and 48 h of incubation, respectively. Moreover, ardisiacrispin (A + B) induced dose-dependent apoptosis of HL-60 cells in the concentration of 1.0-7.5 mg·L-1. Furthermore, the PARP cleavage was detectable in a dose-dependent manner, 2.5 mg·L-1 Ardisiacrispin A+Ardisiacrispin B generated a 27.1% of lysis fraction for 24 h of incubation.
CONCLUSIONS:
Ardisiacrispin A+Ardisiacrispin B exhibits prominent abilities to inhibit the proliferation of HL-60 cells by blocking the cell cycle at S phase and inducing apoptosis.
Fitoterapia. 2011 Jul;82(5):782-5.
A new triterpene saponin from Androsace integra.[Pubmed:
21497642]
METHODS AND RESULTS:
A new triterpene saponin, androsacin (1), along with two known compounds, Ardisiacrispin A (2) and saxifragifolin A (3), were isolated from the whole plants of Androsace integra. The chemical structure of the new compound was elucidated as 3β-O-{β-D-glucopyranosyl-(1→4)-O-β-D-xylopyranosyl-(1→2)-O-β-D-glucopyranosyl-(1→4)-[O-β-D-glucopyranosyl-(1→2)]-α-L-arabinopyranosyl}-16α-hydroxy-13β,28-epoxy-olean-30-al on the basis of spectral evidence.
CONCLUSIONS:
Ardisiacrispin A (2) was cytotoxic toward HepG2 cancer cell with the GI(50) value of 1.56μM.
