Panaxynol

Antiplatelet actions of panaxynol and ginsenosides isolated from ginseng.[Pubmed: 2923911]

Biochim Biophys Acta. 1989 Mar 24;990(3):315-20.

The antiplatelet effect of Panaxynol isolated from the diethyl ether layer was compared with those of ginsenosides from the butanol layer of Panax ginseng.
METHODS AND RESULTS:
Panaxynol (0.1 mg/ml) inhibited markedly the aggregation of washed platelets induced by collagen, arachidonic acid, ADP, ionophore A23187, PAF and thrombin while ginsenosides had no significant effect on the aggregation but ginsenoside Ro (1 mg/ml) inhibited the ATP release of platelets. Less inhibitory effect of Panaxynol was observed in the aggregation of platelet-rich plasma. Thromboxane B2 formation of platelets was inhibited by Panaxynol but not by ginsenosides. The antiplatelet effect of Panaxynol was dependent on the incubation time and the aggregability of platelets inhibited by Panaxynol could not easily be recovered after washing the platelets. In human platelet-rich plasma, Panaxynol prevented secondary aggregation and completely blocked ATP release from platelets induced by epinephrine and ADP. Both Panaxynol and ginsenoside Rg2 inhibited the rise of intracellular calcium caused by collagen.
CONCLUSIONS:
It is concluded that Panaxynol is the most potent antiplatelet agent in ginseng and its mechanism of action is chiefly due to the inhibition of thromboxane formation.

Panaxynol induces neurite outgrowth in PC12D cells via cAMP- and MAP kinase-dependent mechanisms.[Pubmed: 16219303 ]

Chem Biol Interact. 2006 Jan 5;159(1):58-64.

Panaxynol, a polyacetylene ((3R)-heptadeca-1,9-diene-4,6-diyn-3-ol; syn. falcarinol), was isolated from the lipophilic fractions of Panax notoginseng, a Chinese traditional medicinal plant.
METHODS AND RESULTS:
In the present study, we reported the neurotrophic effects of Panaxynol on PC12D cells and mechanism involved in neurite outgrowth of the cells. Panaxynol could morphologically promote neurite outgrowth in PC12D cells, concentration-dependently reduce cell division and up-regulate molecular marker (MAP1B) expression in PC12D cells. Panaxynol induces the elevation of intracellular cAMP in PC12D cells. The neurite outgrowth in PC12D cells induced by Panaxynol could be inhibited by the protein kinase A inhibitor RpcAMPS and by MAP kinase kinase 1/2 inhibitor U0126.
CONCLUSIONS:
These observations reveal that Panaxynol could induce the differentiation of PC12D cells in a process similar to but distinct from that of NGF and the Panaxynol's effects were via cAMP- and MAP kinase-dependent mechanisms.

Antiproliferative effect of panaxynol on RASMCs via inhibition of ERK1/2 and CREB.[Pubmed: 18199429 ]

Chem Biol Interact. 2008 Feb 15;171(3):348-54.

Panaxynol (PNN) occurs in many foods such as carrot, celery, and several reports have shown that it has neuritogenic and neuroprotective properties.
METHODS AND RESULTS:
In this study, we have investigated the antiproliferative effect and the mechanism of PNN on platelet-derived growth factor (PDGF)-BB-induced proliferation of rat aortic vascular smooth muscle cells (RASMCs). PNN significantly inhibited PDGF-BB-induced proliferation and DNA synthesis of RASMCs in a concentration-dependent manner. Flow cytometry analysis showed that PNN blocked the cell cycle progression at the G(1)/S phase. Preincubation of RASMCs with 9 microM PNN resulted in a significant inhibition of PDGF-BB-induced extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylation expression and PDGF-BB-induced CREB phosphorylation expression.
CONCLUSIONS:
The results indicated that the inhibitory effect of PNN on the PDGF-BB-induced proliferation of RASMCs might be mediated by blocking phosphorylation of ERK1/2 and that of CREB.

Inhibitory effects of panaxynol on proliferation of human pancreatic cancer cell PANC-1[Reference: WebLink]

Panaxynol protects cortical neurons from ischemia-like injury by up-regulation of HIF-1alpha expression and inhibition of apoptotic cascade.[Pubmed: 19800326 ]

Chem Biol Interact. 2010 Jan 5;183(1):165-71.

Apoptosis is one of the major characteristics of delayed neuronal degeneration in neuronal injury following cerebral ischemia. Hypoxia-induced apoptosis may be co-regulated by HIF-1alpha as well as many other factors. In recent years, numerous studies concerning Panaxynol (PNN) have been reported. However, whether PNN can show anti-hypoxia properties is still unknown.
METHODS AND RESULTS:
In this study, the protective effects of PNN on OGD-induced neuronal apoptosis and potential mechanisms were investigated. Pretreatment of the cells with PNN for 24h following exposure to OGD resulted in a significant elevation of cell survival determined by MTT assay, LDH assay, Hoechst staining and flow cytometric assessment. In addition to enhancing the expression of HIF-1alpha, PNN also normalized the caspase-3 expression/activation and increased the Bcl-2/Bax ratio. In our study, the increased level of HIF-1alpha with decreased cellular apoptosis suggested an important role for HIF-1alpha in hypoxic neurons.
CONCLUSIONS:
These results indicated that the neuroprotective effects of PNN on hypoxic neurons were at least partly due to up-regulation of HIF-1alpha and raised the possibility that PNN might reduce neurodegenerative disorders and ischemic brain diseases.

Jiangsu Medical Journal, 2015 , 41 (1) :7-10.

To investigate the inhibitory effects of Panaxynol(PNN)on the proliferation of human pancreatic cancer cell PANC-1.
METHODS AND RESULTS:
PANC-1cells were divided into three PNN groups(treated with PNN 1,9and 27μmol/L)and group C(control).The proliferation of PANC-1cells,changes of cell cycle and Ki67 expression were detected by MTT,flow cytometry and Western blot,respectively. Among PNN groups,the inhibition rate and cell proportion in G1 phase were increased and Ki67 expression was reduced in PNN concentration-dependent manner(P0.01).
CONCLUSIONS:
PNN has inhibitory effects on the proliferation of human pancreatic cancer cell PANC-1through inhibiting cell division and down-regulating Ki67 expression.