PanaxatriolCAS# 32791-84-7 |
Quality Control & MSDS
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| Cas No. | 32791-84-7 | SDF | Download SDF |
| PubChem ID | 73599 | Appearance | White powder |
| Formula | C30H52O4 | M.Wt | 476.73 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in methan | ||
| Chemical Name | (3S,5R,6R,8R,9R,10R,12R,13R,14R,17S)-4,4,8,10,14-pentamethyl-17-[(2R)-2,6,6-trimethyloxan-2-yl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthrene-3,6,12-triol | ||
| SMILES | CC1(CCCC(O1)(C)C2CCC3(C2C(CC4C3(CC(C5C4(CCC(C5(C)C)O)C)O)C)O)C)C | ||
| Standard InChIKey | QFJUYMMIBFBOJY-UXZRXANASA-N | ||
| Standard InChI | InChI=1S/C30H52O4/c1-25(2)12-9-13-30(8,34-25)18-10-15-28(6)23(18)19(31)16-21-27(5)14-11-22(33)26(3,4)24(27)20(32)17-29(21,28)7/h18-24,31-33H,9-17H2,1-8H3/t18-,19+,20+,21+,22-,23-,24-,27+,28+,29+,30+/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Panaxatriol is an inducer of thioredoxin-1 (Trx-1), which exhibits anti-inflammatory, hepatoprotective, anti-arrhythmic, and antioxidative activities. It has pluripharmacological properties in the protection against Parkinson's disease (PD) including enhancing antioxidant activity, acting as neurotrophic factor, modulating inflammation and inhibiting mitochondria-mediated apoptosis. Panaxatriol has been shown to be efficacious in the prevention and treatment of cerebrovascular diseases in China, it may activate endogenous cytoprotective mechanism against OGD-Rep induced oxidative injury via the activation of PI3K/Akt and Nrf2 signaling pathway. |
| Targets | COX | Caspase | Nrf2 | HO-1 | PI3K | Akt | VEGFR | HSP (e.g. HSP90) | ATPase |
| In vitro | Panaxatriol saponins extracted from Panax notoginseng induces thioredoxin-1 and prevents 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.[Pubmed: 19857566 ]J Ethnopharmacol. 2010 Feb 3;127(2):419-23.Thioredoxin-1 has various biologic activities, including the control of redox balance and the inhibition of apoptosis. The current study was designed to examine the effects of Panaxatriol saponins (PTS) extracted from Panax notoginseng on thioredoxin-1 expression and 1-methyl-4-phenylpyridinium ion-induced injury.
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| In vivo | The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart.[Pubmed: 20353807]Food Chem Toxicol. 2010 Jun;48(6):1516-20.The aim of the present study was to evaluate the protective effect of ginseng total saponin, panaxadiol and Panaxatriol, which are the major components of Panax ginseng, against myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts.
Protective effect of panaxatriol saponins extracted from Panax notoginseng against MPTP-induced neurotoxicity in vivo.[Pubmed: 20951784 ]J Ethnopharmacol. 2011 Jan 27;133(2):448-53.Panaxatriol saponins (PTS), the main constituents extracted from Panax notoginseng, a Chinese herbal medicine, has been shown to be an effective agent on various diseases. Our previous study has demonstrated that PTS is an inducer of thioredoxin-1 (Trx-1) and has a possible potential as a therapeutic agent for Parkinson's disease (PD). However, the effect of PTS on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in vivo is unknown.
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| Kinase Assay | Panaxatriol saponins attenuated oxygen-glucose deprivation injury in PC12 cells via activation of PI3K/Akt and Nrf2 signaling pathway.[Pubmed: 24955212]Oxid Med Cell Longev. 2014;2014:978034.Panaxatriol saponins (PTS), the main components extracted from Panax notoginseng, have been shown to be efficacious in the prevention and treatment of cerebrovascular diseases in China. NF-E2-related factor 2 (Nrf2), a transcription factor regulating antioxidant and cytoprotective responses to oxidative stress, has received particular attention as a molecular target for pharmacological intervention of ischemic diseases.
The aim of this study was to characterize the effect of PTS on the activation of Nrf2 signaling pathway and the potential role in its protective effect.
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| Animal Research | Protective effects and its mechanism of panaxatriol saponins isolated from Panax notoginseng on cerebral ischemia。[Pubmed: 12774330]Zhongguo Zhong Yao Za Zhi. 2002 May;27(5):371-3.To study the protective effects and its mechanism of Panaxatriol Saponins isolated from Panax notoginseng (PTS) on focal cerebral ischemia in rat brain.
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Panaxatriol Dilution Calculator
Panaxatriol Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.0976 mL | 10.4881 mL | 20.9762 mL | 41.9525 mL | 52.4406 mL |
| 5 mM | 0.4195 mL | 2.0976 mL | 4.1952 mL | 8.3905 mL | 10.4881 mL |
| 10 mM | 0.2098 mL | 1.0488 mL | 2.0976 mL | 4.1952 mL | 5.2441 mL |
| 50 mM | 0.042 mL | 0.2098 mL | 0.4195 mL | 0.839 mL | 1.0488 mL |
| 100 mM | 0.021 mL | 0.1049 mL | 0.2098 mL | 0.4195 mL | 0.5244 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Panaxatriol is a natural product that can relieve myelosuppression induced by radiation injury.
References:
[1]. Liu FY, et al. Effect of panaxatriol on hematogenesis and granulocyte-macrophage colony stimulating factor in radiation injured mice. Saudi Med J. 2007 Dec;28(12):1791-5.
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Panaxatriol saponins extracted from Panax notoginseng induces thioredoxin-1 and prevents 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.[Pubmed:19857566]
J Ethnopharmacol. 2010 Feb 3;127(2):419-23.
AIM OF THE STUDY: Thioredoxin-1 has various biologic activities, including the control of redox balance and the inhibition of apoptosis. The current study was designed to examine the effects of Panaxatriol saponins (PTS) extracted from Panax notoginseng on thioredoxin-1 expression and 1-methyl-4-phenylpyridinium ion-induced injury. MATERIALS AND METHODS: Using PC12 cells and Kunming mice, we test thioredoxin-1 expression after PTS treatment by Western blot. The protective effect of PTS against 1-methyl-4-phenylpyridinium ion-induced injury was assessed by MTT assay and LDH release assay. RESULTS: PTS induced thioredoxin-1 expression in vitro and in vivo, and attenuated 1-methyl-4-phenylpyridinium ion-induced cell death of PC12 cells. CONCLUSIONS: PTS is a new inducer of thioredoxin-1 and has a possible potential as a therapeutic agent for neurodegenerative diseases including Parkinson's disease.
The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart.[Pubmed:20353807]
Food Chem Toxicol. 2010 Jun;48(6):1516-20.
The aim of the present study was to evaluate the protective effect of ginseng total saponin, panaxadiol and Panaxatriol, which are the major components of Panax ginseng, against myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts. Rats were orally administered once a day with total saponin (20 mg/kg), panaxadiol (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.
[Protective effects and its mechanism of panaxatriol saponins isolated from Panax notoginseng on cerebral ischemia].[Pubmed:12774330]
Zhongguo Zhong Yao Za Zhi. 2002 May;27(5):371-3.
OBJECTIVE: To study the protective effects and its mechanism of Panaxatriol Saponins isolated from Panax notoginseng (PTS) on focal cerebral ischemia in rat brain. METHOD: The influences of PTS on cerebral water content and three specific proteins (VEGF, HSP70 and transferrin) related with cerebral ischemia were studied with unilateral occlusion of the middle cerebral artery (MCAO) and Western Blot. RESULT: PTS 12.5 mg.kg-1 i.p. x 7 d (5 d before MCAO and 2 d after MCAO) inhibited the increase of cerebral water content caused by MCAO and influenced contents of HSP70 and transferrin, but had no influence on VEGF protein level. CONCLUSION: PTS shows a protective effect on focal cerebral ischemia in rat brain by alleviating cerebral edema, up-regulating the expression of HSP70, down-regulating transferrin and maintaining blood-brain barrier.
Panaxatriol saponins attenuated oxygen-glucose deprivation injury in PC12 cells via activation of PI3K/Akt and Nrf2 signaling pathway.[Pubmed:24955212]
Oxid Med Cell Longev. 2014;2014:978034.
Panaxatriol saponins (PTS), the main components extracted from Panax notoginseng, have been shown to be efficacious in the prevention and treatment of cerebrovascular diseases in China. NF-E2-related factor 2 (Nrf2), a transcription factor regulating antioxidant and cytoprotective responses to oxidative stress, has received particular attention as a molecular target for pharmacological intervention of ischemic diseases. The aim of this study was to characterize the effect of PTS on the activation of Nrf2 signaling pathway and the potential role in its protective effect. We found that PTS induced heme oxygenase-1 (HO-1) expression in PC12 cells via activating Nrf2 signaling pathway. Phosphatidylinositol 3-kinase (PI3K)/Akt kinase was involved in the upstream of this PTS activated pathway. Moreover, combination of the main components in PTS significantly enhanced the expression of Nrf2 mediated phase II enzymes. Importantly, the protective effect of PTS against oxygen-glucose deprivation-reperfusion (OGD-Rep) induced cell death was significantly attenuated by PI3K inhibitor and antioxidant response element (ARE) decoy oligonucleotides, suggesting that both PI3K/Akt and Nrf2 signaling pathway are essential during this protective process. Taken together, our results suggest that PTS may activate endogenous cytoprotective mechanism against OGD-Rep induced oxidative injury via the activation of PI3K/Akt and Nrf2 signaling pathway.
Protective effect of panaxatriol saponins extracted from Panax notoginseng against MPTP-induced neurotoxicity in vivo.[Pubmed:20951784]
J Ethnopharmacol. 2011 Jan 27;133(2):448-53.
AIM OF THE STUDY: Panaxatriol saponins (PTS), the main constituents extracted from Panax notoginseng, a Chinese herbal medicine, has been shown to be an effective agent on various diseases. Our previous study has demonstrated that PTS is an inducer of thioredoxin-1 (Trx-1) and has a possible potential as a therapeutic agent for Parkinson's disease (PD). However, the effect of PTS on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in vivo is unknown. MATERIALS AND METHODS: Using locomotor activity test and traction test, we detected the effect of PTS on MPTP-induced behavioral impairment. Tyrosine hydroxylase, Trx-1, cyclooxygenase-2, pro-caspase-9, pro-caspase-12 and caspase-3 expressions in the anatomical region of substantia nigra pars compacta (SNc) were tested by Western blot. RESULTS: PTS provided neuroprotection against the loss of dopaminergic neurons and behavioral impairment caused by MPTP. MPTP-induced neuronal death in the SNc was suppressed by PTS through increasing Trx-1 expression, suppressing cyclooxygenase-2 over-expression and inhibiting mitochondria-mediated apoptosis. CONCLUSIONS: PTS, an inducer of Trx-1, has pluripharmacological properties in the protection against PD including enhancing antioxidant activity, acting as neurotrophic factor, modulating inflammation and inhibiting mitochondria-mediated apoptosis.
