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At least 721 records · Page 40Linked to original sources
PubMed2001

Isolation of a novel thermolabile heterodimeric ribonuclease with antifungal and antiproliferative activities from roots of the sanchi ginseng Panax notoginseng.

An isolation procedure, consisting of ion exchange chromatography on CM-Sepharose, affinity chromatography on Affi-gel blue gel, and fast protein liquid chromatography on Mono S, was utilized to purify a base-nonspecific, heterodimeric ribonuclease (RNase) with diverse activities from roots of the sanchi ginseng Panax notoginseng. The RNase is unique in that it consists of two different nonglycoprotein subunits with a molecular weight of 27 and 29 kDa, respectively. The latter subunit is characterized by an N-terminal sequence showing remarkable similarity to that of the bitter gourd RNase. The Panax notoginseng RNase demonstrates potent RNase and translation-inhibitory activities. In addition, it exhibits antiproliferative activity toward leukemia L1210 cells and antifungal activity against Physalospora piricola and Coprinus comatus. Its RNase activity is not heat-resistant, unlike most RNases which are thermostable.

Animals↗
PubMed1996

Pulmonary protective and vasodilator effects of a standardized Panax ginseng preparation following artificial gastric digestion.

We have previously demonstrated that purified ginsenosides produce pulmonary vasodilation and prevent effects of free radical injury on the lung. We examined the effect of artificially digested standardized ginseng preparation G115 in perfused rabbit lungs. G115 was incubated in artificial gastric juice (0.03 M NaCl + 0.08 M HCl) 37 degrees C for 1 h, and artificial intestinal juice (0.05 M KH2PO4 + 0.02 M NaOH) 37 degrees C for 5 h, neutralized with NaOH and lyophilized. Pulmonary vasoconstriction was induced with U46619, and cumulative additions of G115 in undigested, gastric digested and gastric and intestinal digested forms were made to the perfusate. In separate experiments, oxygen free radical injury by electrolysis was produced in the presence of G115 in the perfusate and ACh-induced vasodilation assessed before and after injury. Undigested, gastric digested and combined gastric and intestinal digested G115 significantly dilated lungs (44%, undigested; 26%, gastric digested; 45%, gastric and intestinal digested). In addition, both undigested (-27 +/- 5% vs. -24 +/- 5%) as well as gastric and intestinal digested G115 (-23 +/- 3% vs. -16 +/- 2%) preserved ACh-induced vasodilation following injury. Artificially digested G115 is a pulmonary vasodilator which protects against free radical injury, suggesting that oral G115 has the same effects.

Administration, Oral↗
PubMed2000

Extracts of Ginkgo biloba and Panax ginseng protect brain proteins from free radical induced oxidative damage in vitro.

Oxidative damage to normal human brain tissue was induced following exposure to hydroxyl (OH.) or superoxide (O2-.) free radical species generated by CO60 irradiation in vitro. Both enzymic and cytoskeletal proteins showed substantial (dose dependent) oxidative damage following exposure to OH. or O2-., as quantified by SDS-polyacrylamide gel electrophoretic analysis. Extracts of Ginkgo biloba or Panax ginseng showed a remarkable capacity to protect brain tissue proteins from oxidative damage in vitro, even at extreme (2000 kRads) dosage levels of OH. or O2-.. We suggest, therefore, that the beneficial effect of these plant extracts in preventing brain tissue damage in vivo (e.g. following ischemia-reperfusion) may result from their action in protecting brain proteins from oxidative damage, in addition to their previously reported capacity to reduce free radical induced lipid peroxidation.

Brain Damage, Chronic↗
PubMed1994

High sequence similarity between a ribonuclease from ginseng calluses and fungus-elicited proteins from parsley indicates that intracellular pathogenesis-related proteins are ribonucleases.

A ribonuclease from a callus cell culture of Panax ginseng C.A. Mey strain R1 was isolated. A pure protein with an apparent molecular mass of 18 kDa was obtained. The N-terminal sequences of the protein and of the C-terminal CNBr peptide were determined. No homology with other ribonucleases was found, but there was 60-70% sequence identity with two intracellular pathogenesis-related (IPR) proteins from parsley, indicating that not only these two proteins, but also homologous IPR proteins identified in other plant species are ribonucleases.

Amino Acid Sequence↗
PubMed1999

Inhibitory effect of arginine-derivatives from ginseng extract and basic amino acids on protein-arginine N-methyltransferase.

Protein-arginine N-methyltransferase (protein methylase I) catalyzes methylation of arginyl residues on substrate protein posttranslationally utilizing S-adenosyl-L-methionine as the methyl donor and yields NG-methylarginine residues. Arginyl-fructose and arginyl-fructosyl-glucose from Korean red ginseng were found to inhibit protein methylase I activity in vitro. This inhibitory activity was shown to be due to arginyl moiety in the molecules, rather than that of carbohydrates. Several basic amino acids as well as polyamines were also found to inhibit protein methylase I activity. Interestingly, the intensity of the inhibitory activity was correlated with the number of amino-group in polyamines, thus, in the order of spermine > spermidine > putrescine > agmatine-sulfate, with IC50 at approximately 15 mM, 25 mM, 35 mM, and 50 mM, respectively. On the other hand, neutral amino acids or NaCl did not inhibit the enzyme activity. Lineweaver-Burk plot analysis of the protein methylase I activity in the presence of arginine and spermidine indicated that the inhibition was competitive in nature in respect to protein substrate, with the Ki values of 24.8 mM and 11.5 mM, respectively.

Amino Acids↗
PubMed1984

Immunomodulatory effects of Panax Ginseng C.A. Meyer in the mouse.

An aqueous extract of Panax Ginseng C.A. Meyer (G.S.) was prepared by boiling crushed G.S. roots in water. The extract obtained was adjusted to 125 mg G.S. per ml and was administered orally to mice for 5 to 6 days at the daily dose of 10, 50 and 250 mg G.S. per kg or was added to cultures of mouse spleen cells at concentrations varying between 0.25 and 8 mg G.S. per ml. The average total ginsenoside content of the G.S. roots used was determined by HPLC analysis and found to be 0.58% (w/w). Treated mice responded with enhanced antibody formation to either a primary or a secondary challenge with sheep red cells. The effects were dose-dependent. At the highest dose regimen, the primary IgM response was increased by 50% and the secondary IgG and IgM responses were increased by 50 and 100%, respectively. An even more pronounced effect was obtained with natural killer cell activity which was enhanced between 44 and 150% depending on the effector-to-target cell ratios used in the assay. In vitro, G.S. showed two main effects, an inhibition of stimulated and spontaneous lymphocyte proliferation at high, but not cytotoxic concentrations and an enhancement of interferon production particularly in non-stimulated spleen cells. The immunostimulating effects obtained in vivo are in agreement with the stimulation of interferon production observed in vitro. The inhibition of lymphocyte proliferation, however, cannot be reconciled with the immunostimulatory action of G.S. observed in vivo.

Animals↗
PubMed1991

Effect of Panax ginseng extract on passive avoidance retention in old rats.

Female rats of two groups (6 and 27 months) were tested in the passive avoidance test to investigate the age-dependency of the learning ability. The results showed a significantly better avoidance behavior in the young adult animals compared to the older ones. The influence of a 13-day treatment with Panax ginseng (30 mg/kg/d, oral) on 27 month old rats caused a considerably prolonging of the latency time in comparison to the untreated control group of the same age. In the open field the treated rats exhibited neither an altered locomotion nor exploration nor a changed emotional reactivity which could explain the improved avoidance reaction.

Aging↗
PubMed2005

G1 phase arrest of the cell cycle by a ginseng metabolite, compound K, in U937 human monocytic leukamia cells.

We recently reported that the ginseng saponin metabolite, compound K (20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol, IH901), inhibits the growth of U937 cells through caspase-dependent apoptosis pathway. In this study, we further characterized the effects of compound K on U937 cells and found that, in addition to apoptosis, compound K induced the arrest of the G1 phase. The compound K treated U937 cells showed increased p21 expression; an inhibitory protein of cyclin-cdk complex. The up-regulation of p21 was followed by the inactivation of cyclin D and the cdk4 protein, which act at the early G1 phase, and cyclin E, which acts at the late G1 phase. Furthermore, compound K induced the activation of JNK and the transcription factor AP-1, which is a downstream target of JNK. These findings suggest that the up-regulation of p21 and activation of JNK in the compound K treated cells contribute to the arrest of the G1 phase.

Cyclin D↗
PubMed2006

Antiplatelet and antithrombotic activities of Korean Red Ginseng.

The antiplatelet and antithrombotic activities of Korean Red Ginseng (KRG) were examined on rat carotid artery thrombosis in vivo, and platelet aggregation in vitro and ex vivo. Administration of KRG to rats not only prevented carotid artery thrombosis in vivo in a dose-dependent manner, but also significantly inhibited ADP- and collagen-induced platelet aggregation ex vivo, while failed to prolong coagulation times such as activated partial thromboplastin time (APTT) and prothrombin time (PT), indicating the antithrombotic effect of KRG might be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, KRG inhibited U46619-, arachidonic acid-, collagen- and thrombin-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 620 +/- 12, 823 +/- 22, 722 + 21 and 650 +/- 14 microg/mL, respectively. Accordingly, KRG also inhibited various agonists-induced platelet serotonin secretions as it suppressed platelet aggregation. These results suggest that KRG has a potent antithrombotic effect in vivo, which may be due to antiplatelet rather than anticoagulation activity, and KRG intake may be beneficial to the individuals with high risks of thrombotic and cardiovascular diseases.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

The therapeutic effect of tissue cultured root of wild Panax ginseng C.A. Mayer on spermatogenetic disorder.

This study examined the possibility of using a tissue cultured root of wild Panax ginseng (tcwPG) as a fertility agent. The effect of tcwPG on spermatogenesis was studied using male rats. The tcwPG crude powder was administered orally to 7-week-old rats over a 6-week period. The number of sperm in the testes and epididymides was significantly higher than the control. A histological examination did not reveal any morphological changes in the testes from the tcwPG powder treated rats. Moreover, there were no significant differences in the weights of the heart, spleen, liver, kidney, brain, testes and epididymides. Oligospermia was also induced by administering 2,3,7,8-tetrachlorodaibenzo-p-dioxin (TCDD) to the rats in order to estimate the feasibility of using tcwPG as treatment for infertility caused by spermatogenic disorders. After exposing the rats to TCDD, the tcwPG saponin fraction treated rats showed some improvement in the body weight, sperm number and testis morphology. It was estimated that tcwPG had feasibility as a therapeutic agent on spermatogenic disorder.

Animals↗
PubMed2001

In vitro anti-Helicobacter pylori activity of panaxytriol isolated from ginseng.

This study investigated the effect that some polyacetylenes and protopanaxatriol, which were isolated from heated ginseng (family Araliaceae), have on inhibiting Helicobacter pylori (HP) growth. Among the compounds tested, panaxytriol was quite effective in inhibiting HP growth with an MIC of 50 microg/ml. Ginsenoside Rh1 and protopanaxatriol weakly inhibited H+/K+-ATPase from a rat stomach.

Alkynes↗
PubMed2002

Effect of butanol fraction of Panax ginseng head on gastric lesion and ulcer.

From our previous result that Panax ginseng head extract had inhibition of gastric damages, the extract was fractionated. Among the hexane, chloroform, butanol and water fractions, butanol fraction showed the most potent inhibition of HCl.ethanol-induced gastric lesion, aspirin-induced gastric ulcer, acetic acid-induced ulcer and Shay ulcer. Butanol fraction showed significant increase in mucin secretion, and inhibited malondialdehyde (MDA) and H+/ K+ATPase activity in the stomach. This results indicate that the effectiveness of the fraction on gastric damages might be related to inhibition of acid secretion, increment of mucin secretion and antioxidant property.

Acetic Acid↗
PubMed2002

Epidermis proliferative effect of the Panax ginseng ginsenoside Rb2.

Ginseng has been used as a traditional medicine with various therapeutic effects. However, it is still unknown which component of this plant is effective at promoting wound healing. Recently, ginsenoside Rb2 has been reported to improve wound healing. In this study, to investigate the reported wound healing effect of the ginsenoside Rb2, cell morphology and protein factors involved in epidermal formation were evaluated by immunochemical and immunoblotting analysis. Rb2 stimulated epidermal cell proliferation, and the cell showed a 1.5-fold increase in thymidine uptake compared to the control (p<0.05, n=3). Furtheremore, Rb2 was found to stimulate epidermis formation in a dose-dependent manner in raft culture, and to dose dependently enhance the expressions of protein factors related to cell proliferation, namely, epidermal growth factor and its receptor, fibronectin and its receptor, keratin 5/14, and collagenase I (p<0.05, n=3-9). It is believed that ginsenoside Rb2 enhances epidermal cell proliferation by upregulating the expressions of these proliferation-related factors.

Antineoplastic Agents, Phytogenic↗
PubMed1998

Effect of ginseng total saponin on bovine adrenal tyrosine hydroxylase.

Ginseng total saponin (GTS) can modulate dopaminergic activity at both presynaptic and postsynaptic dopamine receptors (Kim et al., 1998). The present study investigated the effect of GTS on the bovine adrenal tyrosine hydroxylase (TH), which catalyze L/tyrosine to DOP. GTS inhibited the bovine adrenal TH by 42.4, 51.5 and 55.3% at concentrations of 40, 80 and 100 micrograms/ml, respectively. The IC50 value of GTS was 77.5 micrograms/ml. GTS exhibited noncompetitive inhibition with a substrate L-tyrosine. The Ki value was 155 micrograms/ml.

Adrenal Glands↗
PubMed2004

Role of the Fas/Fas ligand death receptor pathway in ginseng saponin metabolite-induced apoptosis in HepG2 cells.

This research team found in previous studies, that the ginseng saponin metabolite IH901 induces apoptosis in HepG2 cells via a mitochondrial-mediated pathway, which resulted in the activation of caspase-9 and subsequently of caspase-3 and -8. Based on these results, the involvement of the Fas/Fas ligand (FasL) death-receptor pathway, in IH901-induced apoptosis in HepG2 cells, was investigated. Levels of Fas and the Fas ligand (FasL) mRNA or protein were not increased by IH901, rather they were decreased significantly at 18 h post treatment. Soluble FasL (sFasL) was detectable by immunoprecipitation analysis in the medium of HepG2 cells treated with IH901. Increased levels of sFasL were inversely correlated with the levels of FasL. Preincubation of HepG2 cells with antagonistic anti-Fas antibody showed little protective effect, if any, on IH901-induced cell death. At a 30 microM (24 and 48 h) and 40 microM (24 h) concentration of IH901, the cytotoxic effect of IH901 was less then 50%, anti-Fas antibody prevented IH901-induced cell death. However, at a 60 microM (24 and 48 h) and 40 microM (48 h) concentration of IH901, cell death rates were about 80% or more and most of the chemopreventive and chemotherapeutic effects of IH901 were manifested. Blocking the Fas receptor did not influence IH901-induced cell death. These results indicate that the Fas/FasL system is engaged, but not required for IH901-induced cell death, at pharmacologically significant concentrations.

Apoptosis↗
PubMed2004

Effects of polysaccharide ginsan from Panax ginseng on liver function.

Ginsan, a polysaccharide isolated from Panax ginseng, has been shown to be a potent immunomodulator, producing a variety of cytokines such as TNF-alpha, IL-1, IL-2, IL-6, IL-12, IFN-gamma and GM-CSF, and stimulating lymphoid cells to proliferate. In the present study, we analyzed some immune functions 1st-5th days after ginsan i.p. injection, including the level of non-protein thiols (NPSH) as antioxidants, heme oxygenase (HO) activity as a marker of oxidative stress, zoxazolamine-induced paralysis time and level of hepatic cytochrome P-450 (CYP450) as indices of drug metabolism system, and activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and albumin level as indicators of hepatotoxicity. Ginsan in the dose of 100 mg/kg caused marked elevation (1.7 to approximately 2 fold) of HO activity, decrease of total CYP450 level (by 20-34%), and prolongation of zoxazolamine-induced paralysis time (by 65-70%), and showed some differences between male and female mice. Ginsan treatment did not seem to cause hepatic injury, since serum AST, ALT, and ALP activities and levels of total bilirubin and albumin were not changed.

Animals↗
PubMed2004

Vascular effects of Siberian ginseng (Eleutherococcus senticosus): endothelium-dependent NO- and EDHF-mediated relaxation depending on vessel size.

Siberian ginseng (SG) has been widely and historically consumed as a health food product for the improvement of self well-being, but whether vascular relaxation may contribute to such a therapeutic health effect has not been studied. We therefore investigated the vasorelaxant effect of the aqueous extract of the roots of SG (Eleutherococcus senticosus Maxim) using several in vitro vascular rings prepared from dog carotid artery, rat aorta and rat mesenteric artery. SG extract (0.04-0.8 mg/ml) caused concentration-dependent relaxation in dog carotid arterial rings pre-contracted with 100 microM phenylephrine (PE), and the relaxation was primarily endothelium-dependent. Treatment with 100 microM L-NOARG (a nitric oxide synthase inhibitor) either prevented or totally reverted SG-induced relaxation, suggesting that the endothelium-dependent relaxation was mediated by NO. Similar endothelium-dependent vascular relaxant responses were also obtained with rat aortic and mesenteric arterial rings, except that it occurred over a relatively higher concentration range of SG (0.5-2.0 mg/ml). When tested in the presence of 300 microM L-NAME, the vasorelaxant effect of SG was inhibited totally in rat aorta but only partially in rat mesenteric artery. The relaxation to SG that was insensitive to L-NAME in rat mesenteric arterial rings was eliminated when the rings (both proximal and distal ends) were pre-treated with a combination of 300 microM L-NAME and 15 mM KCl indicating the involvement of endothelium-derived hyperpolarizing factor (EDHF). This vasorelaxant response of the SG extract was inhibited partially by atropine (1 microM), completely by TEA (5 mM), but not by indomethacin (1 microM) or propranolol (10 microM). SG up to 2 mg/ml had no effect on KCl-induced contraction in any of the vascular rings studied. When compared with carbachol-induced (CCh) relaxation, SG resembles CCh in that the sensitivity to L-NAME inhibition is dependent on vascular size, i.e. aorta >proximal end of mesenteric artery >distal end of mesenteric artery. However, SG exhibited different potencies to relaxation while CCh showed similar potency (EC(50) of about 0.2 microM) in all three vascular segments. In conclusion, we have demonstrated that the vascular effect of SG is endothelium-dependent and mediated by NO and/or EDHF depending on the vessel size. Other vasorelaxation pathways, such as inhibition of K(+)-channels and activation of muscarinic receptors, may also be involved.

Animals↗
PubMed2000

The memory enhancing effects of a Ginkgo biloba/Panax ginseng combination in healthy middle-aged volunteers.

The effects of capsules containing 60 mg of a standardised extract of Ginkgo biloba (GK501) and 100 mg of a standardised extract of Panax ginseng (G115) on various aspects of cognitive function were assessed in healthy middle-aged volunteers. A double blind, placebo controlled, 14 week, parallel group, repeated assessment, multi-centre trial of two dosing regimens, 160 mg b.i.d. and 320 mg o.d. was conducted. Two hundred and fifty-six healthy middle-aged volunteers successfully completed the study. On various study days (weeks 0, 4, 8, 12 and 14) the volunteers performed a selection of tests of attention and memory from the Cognitive Drug Research computerised cognitive assessment system prior to morning dosing and again, at 1, 3 and 6 h later. The volunteers also completed questionnaires about mood states, quality of life and sleep quality. The Ginkgo/ginseng combination was found significantly to improve an Index of Memory Quality, supporting a previous finding with the compound. This effect represented an average improvement of 7.5% and reflected improvements to a number of different aspects of memory, including working and long-term memory. This enhancement to memory was seen throughout the 12-week dosing period and also after a 2-week washout. This represents the first substantial demonstration of improvements to the memory of healthy middle-aged volunteers produced by a phytopharmaceutical.

Adult↗