| Description: |
Panaxydol has anti-cancer activity, can inhibit the growth and apoptosis of cancer cells, the signaling mechanisms involve a [Ca(2+)](i) increase, JNK and p38 MAPK activation, cAMP, MAP kinase and ROS generation through NADPH oxidase and mitochondria. It induces the differentiation in C6 cells, may through a PI 3-K-dependent pathway. |
| In vitro: |
| Molecules. 2011 Jun 29;16(7):5561-73. | | Induction of apoptosis in human promyelocytic leukemia HL60 cells by panaxynol and panaxydol.[Pubmed: 21716177] | Panaxynol and panaxydol are naturally occurring polyacetylenes, isolated from the lipophilic fractions of Panax notoginseng, that exert anti-proliferative effects against malignant cells. However, to the best of our knowledge, no study concerning the inhibitory effects of the two polyacetylenes on cell growth of human promyelocytic leukemia cells has been reported. In this paper, we examined the antiproliferation and proapoptotic effects of panaxynol and panaxydol on HL60 cells and investigated their mechanism of action.
METHODS AND RESULTS:
Cell growth inhibition of panaxynol and panaxydol were determined by trypan blue dye exclusion assays. Apoptosis of cells was revealed by morphological observation, analysis for nuclear DNA distribution and by annexin V-FITC/ PI staining using flow cytometry. It was found that panaxynol and panaxydol markedly inhibited proliferation of HL60 cells in a time- and dose-dependent manner via an apoptotic pathway. In concern with these findings, Western blot analysis showed proteolytic activation of PKCδ, caspase-3 activation and cleavage of poly (ADP [adenosine diphosphate]-ribose) polymerase in HL60 cells treated by panaxynol and panaxydol.
CONCLUSIONS:
In conclusion, panaxynol and panaxydol have profound effects on growth and apoptosis of HL60 cells, suggesting those substances are worthy of further exploration as potential anti-cancer agents. | | Yakugaku Zasshi. 2011;131(6):993-1000. | | Induction of differentiation by panaxydol in human hepatocarcinoma SMMC-7721 cells via cAMP and MAP kinase dependent mechanism.[Pubmed: 21628989] | Panaxydol (PND) is one of the main non-peptidyl small molecules isolated from the lipophilic fractions of Panax notoginseng.
METHODS AND RESULTS:
The present study was carried out to demonstrate the potential effects of Panaxydol on the induction of differentiation of human liver carcinoma cell lines SMMC-7721. Cell viability was evaluated by MTT method and Trypan blue exclusion assay respectively. The changes of morphology were detected by transmission electron microscope. Inhibitors were applied to detect the signaling pathway of differentiation. The level of intracellular cyclic AMP was determined by radioimmunoassay. The expression of p-ERK, Id1, and p21 were determined by Western blot. We found that Panaxydol inhibit the proliferation of SMMC-7721 cells and caused the morphology and ultrastructure changes of SMMC-7721. Moreover, Panaxydol dose-dependently increased the secretion of albumin and alkaline phosphatase activity, and decreased the secretion of AFP correspondingly. These changes of differentiation markers in SMMC-7721 can be reversed by the protein kinase A inhibitor RpcAMPS and by MAP kinase kinase 1/2 inhibitor U0126 or sorafenib. Intracellular cAMP was elevated by Panaxydol in SMMC-7721 cells.
CONCLUSIONS:
Panaxydol dose-dependently decreased the expression of regulatory factors Id1 and increased the protein levels of p21 and p-ERK1/2 correspondingly. It suggested Panaxydol might be of value for further exploration as a potential anti-cancer agent via cAMP and MAP kinase-dependent mechanism. |
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