Panaxatriol

J Ethnopharmacol. 2010 Feb 3;127(2):419-23.

Panaxatriol saponins extracted from Panax notoginseng induces thioredoxin-1 and prevents 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.[Pubmed: 19857566 ]

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.
CONCLUSIONS:
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. 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.

Food Chem Toxicol. 2010 Jun;48(6):1516-20.

The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart.[Pubmed: 20353807]

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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.

J Ethnopharmacol. 2011 Jan 27;133(2):448-53.

Protective effect of panaxatriol saponins extracted from Panax notoginseng against MPTP-induced neurotoxicity in vivo.[Pubmed: 20951784 ]

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.
METHODS AND RESULTS:
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. 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.

Oxid Med Cell Longev. 2014;2014:978034.

Panaxatriol saponins attenuated oxygen-glucose deprivation injury in PC12 cells via activation of PI3K/Akt and Nrf2 signaling pathway.[Pubmed: 24955212]

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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.

Zhongguo Zhong Yao Za Zhi. 2002 May;27(5):371-3.

Protective effects and its mechanism of panaxatriol saponins isolated from Panax notoginseng on cerebral ischemia。[Pubmed: 12774330]

To study the protective effects and its mechanism of Panaxatriol Saponins isolated from Panax notoginseng (PTS) on focal cerebral ischemia in rat brain.
METHODS AND RESULTS:
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. 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.
CONCLUSIONS:
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.