ABSTRACT
Objective To develop a method for the separation and preparation panaxynol. Methods Panax Notoginseng was extracted by SEF-CO_2, and absorbed by silica gel to remove most of the polar impurities. Panaxynol was preparated with RP-HPLC. Result Panaxynol was identified by UV、IR、MS、NMR,and the purity of panaxynol reached 98%. Conclusion The developed method is simple, reproducible and easy to operate. The solvent is cheap,with low boiling point and easy to recovery property.
ABSTRACT
Aim To evaluate the inhibitory effect of panaxynol(PNN) on the proliferation of rat aortic smooth muscle cell(RASMC) and its mechanisms.Methods Cell proliferation was determined using cell count and -TdR incorporation test.Fura-3/AM and confocal were used to measure intracelluar free Ca~(2+) concentration.Expression of mitochondrial transcription factor 1(mtTF1) mRNA was tested by using RT-PR.Results PNN inhibited the RASMC proliferation and DNA synthesis induced by serum and PDGF-BB in a dose-dependent manner.9 ?mol?L~(-1) of PNN inhibited the increase of intracelluar free Ca~(2+) concentration induced by PDGF-BB.PDGF-BB upregulated the expression of mtTF1 mRNA,which could be suppressed by 3,9 ?mol?L~(-1) of PNN significantly.Conclusions PNN can inhibit RASMC proliferation significantly,which might be related to the decrease of intracellular free Ca~(2+) concentration and mtTF1 mRNA expression.
ABSTRACT
Panax ginseng roots have long been used as a medicinal herb in oriental countries. We have investigated anti-proliferative effects of lipid soluble Panax ginseng components on human renal cancer cell lines. Petroleum ether extract of Panax ginseng roots (GX-PE) or its partially purified preparation (7:3 GX) was added to cultures of three human renal cell carcinoma (RCC) cell lines, A498, Caki-1, and CURC II. Proliferation of RCC cells was estimated by a [3H]thymidine incorporation assay and cell cycle distribution was analyzed by flow cytometry. GX-PE, 7:3 GX, panaxydol and panaxynol inhibited proliferation of all three RCC cell lines in a dose dependent manner in vitro with an order of potency, 7:3 GX > panaxydol > panaxynol = GX-PE. Additive effect of interleukin 4 was also demonstrated, most prominently in Caki-1 which responded poorly to GX-PE alone. Analysis of cell cycle in CURC II and Caki-1 treated with GX-PE demonstrated increase in G1 phase population and corresponding decrease in S phase population. The present study demonstrated that proliferation of human RCC cell lines were inhibited by lipid soluble components of Panax ginseng roots by blocking cell cycle progression at G1 to S phase transition.
Subject(s)
Humans , Alkanes , Alkynes/therapeutic use , Antineoplastic Agents/therapeutic use , Antineoplastic Agents, Phytogenic/therapeutic use , Carcinoma, Renal Cell/drug therapy , Cell Cycle/drug effects , Fatty Alcohols/therapeutic use , Panax/therapeutic use , Panax/chemistry , Interleukin-4/therapeutic use , Kidney Neoplasms/drug therapy , Plant Extracts/therapeutic use , Plant Roots/therapeutic use , Plant Roots/chemistryABSTRACT
Objective To investigate the neuroprotective effect of panaxynol on primary cultured cortical neuron against oxidative stress. Methods Viability of panaxynol acted on neuron oxidative stress was monitored by MTT assay and FCM method. Scavenging effects of panaxynol on free radicals were observed in vitro. Effects of panaxynol on SOD activity and GSH-Px, and MDA content in primary neuron injured by H_2O_2 were also determined. Results Panaxynol (2—16 ?mol/L) could dose-dependently protect neuron from oxidative stress induced by H_2O_2; 8 ?mol/L of panaxynol could decrease necrosis and apoptosis rate of neuron significantly (P