商品描述

Ginseng Roots Extract:

Ginseng Roots Extract was refined from the underground pan (Root and Fibrous root) of ginseng, which belongs to the araliaceae plants. It was a yellow-black powder. The water solubility was 100%. The ginseng root extract not only contained the 29 monosomic saponins of ginseng root, but also contained ginseng polysaccharides, ginseng proteins, glucoproteins, amino acids, ginseng volatile oils, organic germanium and trace elements, etc.
The study had revealed that the ingredients of Ginseng Roots Extracts were similar with that of the ginseng. The ginseng root extract had all the efficiencies of ginseng.
There were many chemical ingredients in ginseng. And each bad its own character with respect to pharmacology. Ginseng saponin could inhibit the lipide peroxides formation in the brain and liver, decrease the free radicals production in the body, and excite the central nervous system. It had the functions such as antifatigue, antiaging and body immunity enhancing. The ginseng glucoprotein had the effect of antivirus. The ginseng protein also had the effects of promoting the formation of neurite and increasing the quantities of brain cells. The ginseng polysaccharide could enhance the body immunity; therefore it could be used as the adjuvant to treat the carcinoma. It could apparently inhibit the liver injury, which was caused by carbon tetroxide, and lower the level of blood sugar The regulation with ginseng to the function and metabolism of the body was a bi-directional adjustment, which was mainly towards facilitating the body function recovering and strengthening, Therefore this regulation was mainly about to improve the body hypofunction caused by intrinsic factors (senescence, etc.) and extrinsic factors (stress. environmental drugs stimulation, etc.), while it had little effects to the normal body. For example, the ginseng root extract could regulate the abnormal blood sugar level, but had no apparent effect to the normal blood sugar level. It could be used to prevent and treat the body hypofuncfion. For there were many ginseng target organs, ginseng root extract was more suitable for the middle and old age person whose organ functions had been declined It was the most ideal health food for these people.
Ginseng Roots Extract conserved most effective parts of ginseng ingredients, such as ginseng root saponins, ginseng polysaccharides, ginseng glucoproteins and phenols For example, the ginseng saponin content was 6-30% (detected by HPLC method), the ginseng polysaccharide content was 24% (detected by UV method), the content of ginseng proteins and amino acids were 15% 8%,respectively.
Compared with the Ginseng Leaves Extract, Ginseng Roots Extract not only could reinforce the efficiency and supply the ingredients which was not existed with the saponins in ginseng stem and leaf but also had the character of easy solubilization in water Therefore the body could easily absorb it. Ginseng Root Extract could be widely used in the areas of medicine and health, such as being made into Ginseng Roots Extract nutrition supplements by filling it into capsule or compacting it into pallet.

Ginseng Leaves Extract：

Ginseng Leaves Extract was refined from the stein and leaf of ginseng, which belongs to the araliaceae plants. It was a white powder and mainly contained eighteen ginseng monosomic saponins. It could be solubilized in 80¡æ water and ethanol.
The main ingredient in Ginseng Leaves Extract was ginseng saponin. Its content could reach 80% (detected by UV method), over 50% (detected by UV method). The experiment results had revealed that the saponin in ginseng stem and leaf could apparently inhibit the formation of lipide peroxide in the brain and liver, reduce the content of the lipofuscin in the cerebral cortex and liver, and at the same time increase the content of superoxide dismutase and catalase in the blood, these results indicated that the saponin in the ginseng stalk and leaf had the effect of antioxidation. In addition, some monomer saponins in ginseng like Rbl. Rb2. Rd, Rc, Re, Rgl, Rg2. and Rhl could reduce the content of free radicals in variable degrees. The ginseng saponin could delay the senescence of nerve cells and decrease the happening rate of memory injury in the aged. These results suggested that the ginseng saponins had tile effects of stabilizing the membrane structure, promoting the synthesis of protein, and increasing the memory ability with the aged.

In Vitro Effect of Standardized Ginseng Extracts and Individual Ginsenosides on the Catalytic Activity of Human CYP1A1, CYP1A2, and CYP1B1:

Ginseng extract has been reported to decrease the incidence of 7,12-dimethylbenz[a]anthracene (DMBA)-initiated tumorigenesis in mice. A potential mechanism for this effect by ginseng is inhibition of DMBA-bioactivating cytochrome P450 (P450) enzymes. In the present in vitro study, we examined the effect of a standardized Panax ginseng (or Asian ginseng) extract (G115), a standardized Panax quinquefolius (or North American ginseng) extract (NAGE), and individual ginsenosides (Rb1, Rb2, Rc, Rd, Re, Rf, and Rg1) on CYP1 catalytic activities, as assessed by 7-ethoxyresorufin O-dealkylation. G115 and NAGE decreased human recombinant CYP1A1, CYP1A2, and CYP1B1 activities in a concentration-dependent manner. Except for the competitive inhibition of CYP1A1 by G115, the mode of inhibition was the mixed-type in the other cases. A striking finding was that NAGE was 45-fold more potent than G115 in inhibiting CYP1A2. Compared with G115, NAGE also preferentially inhibited 7-ethoxyresorufin O-dealkylation activity in human liver microsomes. Rb1, Rb2, Rc, Rd, Re, Rf, and Rg1, either individually or as a mixture and at the levels reflecting those found in an inhibitory concentration (100 µg/ml) of NAGE or G115, did not influence CYP1 activities. However, at a higher ginsenoside concentration (50 µg/ml), Rb1, Rb2, Rc, Rd, and Rf inhibited these activities. Overall, our in vitro findings indicate that standardized NAGE and G115 extracts, which were not treated with calf serum or subjected to acid hydrolysis, inhibited CYP1 catalytic activity in an enzyme-selective and extract-specific manner, but the effects were not due to Rb1, Rb2, Rc, Rd, Re, Rf, or Rg1.

Fig. 1. Content of individual ginsenosides in G115 and NAGE. The content (% w/w) of Rb1,Rb2,Rc,Rd,Re,Rf,Rg1,and Rg2 in the standardized G115 and NAGE extracts were quantified by HPLC, and the data were provided by our suppliers of G115 (Pharmaton S.A.) and NAGE (Canadian Phytopharmaceuticals Corp.).

7-Ethoxyresorufin O-Dealkylation Assay:

7-Ethoxyresorufin O-dealkylation activity was determined by a modification  of a continuous spectrofluorometric assay. Briefly, each standard 2-ml incubation contained 100 mM potassium phosphate buffer, pH 7.4, 5 mM MgCl2, 1.5 mM EDTA, 0.2 µM 7-ethoxyresorufin (unless indicated otherwise), human recombinant P450 enzyme (1 pmol of CYP1A1, 3 pmol of CYP1A2, or 2.5 pmol of CYP1B1) or human liver microsomes (75 pmol of total microsomal P450), and 0.25 mM NADPH. Reaction was performed at 37°C and initiated by the addition of NADPH. Fluorescence was recorded every 30 s for 3 min using a Shimadzu model RF-540 spectrofluorometer. The excitation wavelength was set at 530 nm (5-nm slit width), and the emission wavelength was set at 582 nm (5-nm slit width). Calibration curves were constructed by determining the fluorescence in incubations containing known amounts of the authentic resorufin metabolite. Samples containing the authentic standard were processed in the same manner as the unknown samples but in the presence of heat-inactivated human liver microsomes or control insect cell microsomes.

Fig. 2. Concentration-dependent effect of G115 and NAGE on the catalytic activity of CYP1A1, CYP1A2, and CYP1B1.7-Ethoxyresorufin O-dealkylation assay (0.2 µM substrate concentration) was performed with human recombinant CYP1A1 (A), CYP1A2 (B), and CYP1B1 (C), and varying concentrations of G115 and NAGE. Control incubations contained the vehicle (100 mM potassium phosphate, pH 7.4). Shown are mean ± S.E.M. percentages of control activity for three independent experiments. Control enzyme activity (mean ± S.E.M.) for CYP1A1, CYP1A2, and CYP1B1 was 62 ± 1, 5.1 ± 0.3, and 14 ± 0.4 nmol/min/nmol of P450, respectively.

Fig. 3.   Lineweaver-Burk plots for the inhibition of CYP1A1, CYP1A2, and CYP1B1 by G115. 7-Ethoxyresorufin O-dealkylation assay was performed with human recombinant CYP1A1 (A), CYP1A2 (B), or CYP1B1 (C) at multiple concentrations of 7-ethoxyresorufin (0.025-0.2 µM for CYP1A1 and CYP1B1; 0.1-0.8 µM for CYP1A2) and G115 (125-500 µg/ml for CYP1A1; 500-1500 µg/ml for CYP1A2; 75-225 µg/ml for CYP1B1). The plots were generated by nonlinear regression analysis of the experimental data, as described under Materials and Methods. Results are expressed as mean ± S.E.M. of reciprocal enzyme activity for three independent experiments.

Fig. 4. Lineweaver-Burk plots for the inhibition of CYP1A1, CYP1A2, and CYP1B1 by NAGE. 7-Ethoxyresorufin O-dealkylation assay was performed with human recombinant CYP1A1 (A), CYP1A2 (B), or CYP1B1 (C) at multiple concentrations of 7-ethoxyresorufin (0.025-0.2 µM for CYP1A1 and CYP1B1; 0.1-0.8 µM for CYP1A2) and NAGE (125-500 µg/ml for CYP1A1; 5-20 µg/ml for CYP1A2; 25-100 µg/ml for CYP1B1). The plots were generated by nonlinear regression analysis of the experimental data, as described under Materials and Methods. Results are expressed as mean ± S.E.M. of reciprocal enzyme activity for three independent experiments.

Fig. 5. Effect of G115 and NAGE on 7-ethoxyresorufin O-dealkylation activity in individual human liver microsomes.7-Ethoxyresorufin O-dealkylation activity was determined in a panel of four individual human liver microsome samples (denoted as HG23, HG30, HG56, and HG89) in the presence of G115 or NAGE (each at 60 µg/ml). Control incubations contained the vehicle (100 mM potassium phosphate, pH 7.4). Results are expressed as mean ± S.E.M. of enzyme activity for three independent experiments. *, significantly different from the control, p < 0.05.