Panaxadiol

Catalogue number C108857
Chemical namePanaxadiol
CAS Number19666-76-3
Synonyms(3S,5R,8R,9R,10R,12R,13R,14R,17S)-4,4,8,10,14-pentamethyl-17-[(2R)-2,6,6-trimethyl-2-oxanyl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthrene-3,12-diol
Molecular WeightC30H52O3
Formula460.7
Purity98%
Physical DescriptionWhite powder
SolventChloroform, Dichloromethane,DMSO
StorageStored at 2-8°C, Protected from air and light, refrigerate or freeze
Applications

Rats were orally administered once a day with total saponin (20 mg/kg), Panaxadiol (PD) (5 mg/kg) and panaxatriol (5 mg/kg) for consecutive 7 days. On day 8, the hearts were isolated and perfused with Krebs-Henseleit bicarbonate buffer solution using Langendorff apparatus. After 30 min of global ischemia, hearts were reperfused for 30 min. Myocardial function, coronary flow and biochemical parameters, such as lactate dehydrogenase (LDH), creatine kinase (CK), adenosine triphosphate (ATP), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Total saponin and panaxatriol significantly improved I/R-induced myocardial dysfunction by increasing left ventricular development pressure, (-dP/dt)/(+dP/dt) and time to contracture. Moreover, the increases in the levels of LDH, CK and MDA and the decrease in the levels of GSH were attenuated by total saponin and panaxatriol. However, the ATP levels did not affected by total saponin, panaxadiol and panaxatriol pretreatment. Our findings suggest that pretreatment with ginseng total saponin, especially panaxatriol, ameliorates I/R-induced myocardial damage and this protection is caused by reducing oxidative stress.


Cell growth was markedly suppressed in HCT-116 cells treated by 5-fluorouracil (5-FU) (20-100 microM) for 24 or 48 h with time-dependent effects. The significant suppression on HCT-116 cell proliferation was observed after treatment with Panaxadiol (PD) (25 microM) for 24 and 48 h. Panaxadiol (25 microM) markedly (P < 0.05) enhanced the anti-proliferative effects of 5-FU (5, 10, 20 microM) on HCT-116 cells compared to single treatment of 5-FU for 24 and 48 h. Flow cytometric analysis on DNA indicated that PD and 5-FU selectively arrested cell cycle progression in the G1 phase and S phase (P < 0.01), respectively, compared to the control condition. Combination use of 5-FU with PD significantly (P < 0.001) increased cell cycle arrest in the S phase compared to that treated by 5-FU alone. The combination of 5-FU and PD significantly enhanced the percentage of apoptotic cells when compared with the corresponding cell groups treated by 5-FU alone (P < 0.001). Panaxadiol enhanced the anti-cancer effects of 5-FU on human colorectal cancer cells through the regulation of cell cycle transition and the induction of apoptotic cells.

References

1. Archives of Pharmacal Research, 2008, 31(2), 154-159.

2. Food Chem. Toxicol., 2010, 48(6), 1516-1520.

3. Cancer Chemother Pharmacol., 2009, 64(6), 1097-1104.

4. Carcinogenesis, 2003, 24(11), 1767-1772.

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Panaxadiol
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