| In vitro: |
| Biochim Biophys Acta. 1989 Mar 24;990(3):315-20. | | Antiplatelet actions of panaxynol and ginsenosides isolated from ginseng.[Pubmed: 2923911] | 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. | | Chem Biol Interact. 2006 Jan 5;159(1):58-64. | | Panaxynol induces neurite outgrowth in PC12D cells via cAMP- and MAP kinase-dependent mechanisms.[Pubmed: 16219303 ] | 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. |
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