Lipid-soluble ginseng extract was prepared by n-hexane extraction of red ginseng. BALB/c-nu mice were inoculated with human lung cancer (NCI-H460) cells to establish a human tumor xenograft model in nude mice, and the lipid-soluble ginseng extract was orally administered. The tumor inhibitory rates of the lipid-soluble ginseng extract at doses of 0.1, 0.3, and 1.0 g/kg/day were 18.9% (P < .05), 60.0% (P < .001), and 67.5% (P < .001), respectively. The oral administration of the lipid-soluble extract of red ginseng showed a potent anticancer effect in nude mice bearing human lung cancer cells in a dose-dependent manner without any apparent toxicity. This lipid-soluble ginseng extract is a potential nontoxic anticancer supplement for the prevention and intervention of lung tumor growth through an oral administration route.

The anticancer activity of ginseng originated mainly from lipid-soluble components. The hexane extract of ginseng marc (HEGM) showed a potent inhibitory activity on human hepatoma (HepG2, GI 50 = 41.7 lg/ml) and breast (MCF-7, GI 50 = 54.4 lg/ml) cancer cell proliferation in vitro in a concentration-dependent manner as did the hexane extract of ginseng (HEG), with GI 50 values of 21.1 lg/ml in HepG2 and 41.2 lg/ml in MCF-7. The water extract of ginseng (WEG) possessed a low anticancer activity against both cancer cell lines, but the hexanesoluble fraction of WEG (HSF/WEG) showed a potent anticancer activity against HepG2 (GI 50 = 38.7 lg/ml) and MCF-7 cells (GI 50 = 51.1 lg/ml). The hexane extraction in ginseng was a very promising protocol for the maximum recovery of the anticancer active components in high concentrations. Also the adoption of hexane extraction after water extraction of ginseng was successful in the effective utilization of the residual lipid-soluble anticancer active components in ginseng marc.

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The concentration of cardiac troponin I (cTnI) in blood is an important marker for heart muscle cell damage. A surface plasmon resonance (SPR)-based immunosensor was devised for the rapid and specific detection of cTnI. It was constructed by crosslinking a monoclonal antibody P-II-13, which was generated against a loop region (aa 84-94) of cTnI protein as an epitope peptide, onto a chemically modified thin gold film. The performance of the sensor was examined with respect to the SPR signal intensity versus cTnI concentration. The signal intensity was directly correlated with the cTnI concentration in the range of 0-160 μg/l. The sensor signal was saturated when the concentration of cTnI approached 660 μg/l with the SPR intensity of 172 RU. The lower detection limit of the sensor was 68 ng/l cTnI, which was comparable to ELISA-based commercial cTnI detection systems.

Based on the use of Panax ginseng C.A. Meyer (Family Araliaceae) for the treatment of stroke in traditional Korean medicine, the present study was carried out to evaluate neuroprotective effects of P. ginseng after transient global cerebral ischemia using the four-vessel occlusion rat model. Nissl staining, lipid peroxidation (malondialdehyde [MDA] formation), and activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) of rat brain were assessed. Ethanolic P. ginseng extract (200 mg/kg, i.p.) significantly protected CA1 neurons against 10 minutes of transient forebrain ischemia as demonstrated by measuring the density of neuronal cells. P. ginseng also significantly decreased the level of MDA and increased the expression of GPx and SOD. These results suggest that P. ginseng might be neuroprotective against cerebral ischemia-induced injury in rat brain by decreasing lipid peroxides and increasing the expression of GPx and SOD.

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This study was performed to elucidate the anticancer mechanism of a lipid-soluble ginseng extract (LSGE) by analyzing induction of apoptosis and arrest of cell cycle progression using the NCI-H460 human lung cancer cell line. Proliferation of NCI-H460 cells was potently inhibited by LSGE in a dose-dependent manner. The cell cycle arrest at the G0/G1 phase in NCI-H460 cells was induced by LSGE. The percentage of G0/G1 phase cells significantly increased, while that of S phase cells decreased after treatment with LSGE. The expression levels of cyclin-dependent kinase2 (CDK2), CDK4, CDK6, cyclin D3 and cyclin E related to G0/G1 cells progression were also altered by LSGE. In addition, LSGE-induced cell death occurred through apoptosis, which was accompanied by increasing the activity of caspases including caspase-8, caspase-9 and caspase-3. Consistent with enhancement of caspase activity, LSGE increased protein levels of cleaved caspase-3, caspase-8, caspase-9, and poly-ADP-ribose polymerase (PARP). These apoptotic effects of LSGE were inhibited by the pan-caspase inhibitor Z-VAD-fmk. These findings indicate that LSGE inhibits NCI-H460 human lung cancer cell growth by cell cycle arrest at the G0/G1 phase and induction of caspase-mediated apoptosis.

Potentiometric properties of hydrophilic polyurethane (HPU) coated AgaAgCl electrodes of the second kind have been examined. Three types of HPUs which have 42% (HPU-A), 100% (HPU-B), and 206% (HPU-C) of water uptake have been used as coating membranes for AgaAgCl electrodes. Both HPU coated and bare AgaAgCl electrodes exhibited virtually the same potentiometric response to chloride. On the other hand, all the electrodes exhibited a three step response to bromide; fast initial response to bromide, followed by gradual potential changes (from ±2 to ±25 mVamin), and an abrupt potential drop (between about ±60 and ±80 mV) after some period of time. Fitting the potentiometric response curves to the diffusion model proposed initially by Hulanicki and Lewenstam, and modi®ed later by Morf, it was possible to estimate the relative permeability of HPU membranes: the concentration of bromide that reached the surface of AgCl layer from the bulk solution was reduced by a factor of 1a20 with HPU-A, 1a12 with HPU-B and 1a3 with HPU-C membrane. The ratio of peak currents measured at the HPU coated Pt electrode and that at the bare Pt electrode for various neutral and anionic species indicated that the HPU membranes effectively discriminate the passage of those molecules by their size (e.g., M w`4 00 for neutral and M w`2 00 for anionic molecules). As the HPU membranes substantially reduce the diffusion of larger anions than chloride, e.g., bromide and thiocyanate, the HPU modi®ed AgaAgCl electrodes accurately determine the chloride level in clinical samples even in the presence of those interfering anions. Since the HPU membrane also effectively prevent the surface fouling of the electrode from protein adsorption, the HPU coated AgaAgCl electrode was successfully employed to measure the chloride in serum or whole blood.