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At least 19 recordsLinked to original sources
PubMed2004

[Effect of the sustained release excipients on the release rate of ginsenoside Rg1 and ginsenoside Rb1 in sustained-release tablet of Panax notoginsenosides].

OBJECTIVE: To study the influence of the sustained release excipient on the release rate of ginsenoside Rg1 and ginsenoside Rb1 in sustained-release tablet of Panax Notoginsenosides. METHOD: The release rate of ginsenoside Rg1 and ginsenoside Rb1 in different matrix tablets with different excipient (HPMC, EC), different viscosity of EC (RT-50, RT-100), different ratio of EC in matrix tablet were detected. RESULT: All above different factors influence the release rate of ginsenoside Rg1 and ginsenoside Rb1 and brought them different release curve. CONCLUSION: Emphasis should be laid on the different release characteristic of different active compounds in active fraction.

Chemistry, Pharmaceutical↗
PubMed2006

Activation of insulin-like growth factor I receptor-mediated pathway by ginsenoside Rg1.

Ginsenoside Rg1, an active ingredient in ginseng, was previously shown to be a novel class of potent phytoestrogen. The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF-7) cells. Rg1 (1 pM) stimulates cell proliferation (P<0.01) and estrogen-responsive pS2 mRNA expression (P<0.05) without alteration of estrogen receptor alpha (ERalpha) protein or mRNA expression in MCF-7 cells. In addition, 10(-14)-10(-4) M of Rg1 does not demonstrate specific binding to ERalpha. We hypothesize that Rg1 may exert its actions in MCF-7 cell via the activation of crosstalk between ER- and insulin growth factor I receptor (IGF-IR)-dependent pathways. The results indicate that Rg1 significantly increases IGF-IR expression and IGF-IR promoter activity in MCF-7 cells (P<0.05). Cotreatment of MCF-7 cells with 1 muM of estrogen antagonist ICI 182,780 completely abolishes the effects of Rg1 on IGF-IR expression.Furthermore, Rg1 enhances tyrosine phosphorylation of IRS-1 in MCF-7 cells upon IGF-I stimulation and the activation of IRS-1 phosphorylation is also ER-dependent. Taken together, our results suggest that Rg1 not only increases IGF-IR expression but also enhances IGF-IR-mediated signaling pathways in MCF-7 cells. The stimulation of IGF-IR expression by Rg1 in MCF-7 cells appears to require ER, and its actions might involve ligand-independent activation of ER.

Cell Line↗
PubMed2000

Metabolism of ginsenoside Rg1 by intestinal bacteria. II. Immunological activity of ginsenoside Rg1 and Rh1.

AIM: To compare the effect of ginsenoside Rg1 and its metabolite Rh1 on proinflammatory cytokines and their mRNA expression by THP-1 cells. METHODS: Human peripheral blood mononuclear cells (PBMC) were incubated with Rg1 and Rh1 at concentrations of 0.1, 1, 10, and 100 mg/L, and the cell proliferation was measured 24 h after incubation. Radioimmunoassay (RIA) was used to detect the production of proinflammatory cytokines, TNF alpha, IL-1 alpha, and IL-8. TNF alpha mRNA level was detected by reverse transcription polymerase chain reaction (RT-PCR) after administration of Rg1 and Rh1. RESULTS: Rg1 and Rh1 (at concentration of 0.1, 1, 10, 100 mg/L) had no effect on PBMC proliferation. Rh1 1 mg/L could upregulate the productions of TNF (and IL-8 induced by lipopolysaccharides (LPS) 10 mg/L plus phorbol myristate acetate (PMA) 200 nmol/L, however, Rg1 showed an inhibitory effect on TNF alpha production induced by LPS 100 mg/L. Rg1 1 mg/L and Rh1 100 mg/L enhanced the production of IL-1 alpha level in THP-1 cells in the presence of LPS 10 mg/L. RT-PCR revealed that Rh1 stimulated TNF alpha mRNA expression in suitable stimulatory conditions. CONCLUSION: Rg1 and Rh1 have different effects on the production of cytokines produced THP-1 cells stimulated by LPS and PMA.

Ginsenosides↗
PubMed1990

Immunomodulating activity of ginsenoside Rg1 from Panax ginseng.

The immunomodulatory activity of ginsenoside Rg1 from Panax ginseng was studied in mice using sheep red cells as the antigen. It was found that ginsenoside Rg1 at a dose of 10 mg/kg administered for three consecutive days before immunization increased the number of spleen plaque-forming cell, the titers of sera hemagglutinins as well as the number of antigen-reactive T-cells. Ginsenoside Rg1 also increased the number of T-helper cells with respect to the whole T-cell number and the splenocyte natural killer activity. Ginsenoside Rg1 induced an augmentation of the production of IL-1 by macrophages and exerted a direct mitogenic effect on microcultured thymus cells. Ginsenoside Rg1 also partly restored the impaired immune reactivity by cyclophosphamide treatment.

Animals↗
PubMed2002

Estrogen-like activity of ginsenoside Rg1 derived from Panax notoginseng.

Ginsenosides have demonstrated pharmacological effects in the central nervous, cardiovascular, and endocrine systems. We hypothesize that ginsenosides might mediate some of their actions by binding to the estrogen receptor, as they share many of the protective actions of estrogen in various physiological systems. The present study is aimed to determine whether ginsenoside Rg1 can act like an estrogen analog in stimulating human breast cancer cell growth as well as in the activation of estrogen response element-luciferase activity in HeLa cell. Rg1, but not its aglycone, stimulates [methyl-(3)H] thymidine incorporation in estrogen receptor-positive MCF-7 in a dose-dependent manner (10(-15)-10(-7) M). The stimulation of MCF-7 cell proliferation by 3 x 10(-13) M Rg1 can be blocked by 10(-6) M of the estrogen antagonist ICI 182780. Moreover, Rg1 stimulates estrogen response element-luciferase reporter gene activity in HeLa cells with an optimal dose of 3 x 10(-10) M. Such stimulation can also be blocked by 10(-6) M ICI 182780. In addition, Rg1 has no effect on [methyl-(3)H]thymidine incorporation in estrogen receptor-negative human breast cancer cells (MDA-MB-231). Furthermore, Rg1 failed to displace the specific binding of [(3)H]17 beta-estradiol to MCF-7 cell lysates, suggesting that no direct interaction of Rg1 with estrogen receptor is needed for its estrogenic action. Our results indicate that ginsenosides Rg1 has estrogen-like activity and should be classified as a novel class of potent phytoestrogen.

Breast Neoplasms↗
PubMed2006

Proteomic analysis effects of ginsenoside Rg1 on human umbilical vein endothelial cells stimulated by tumor necrosis factor-alpha.

Ginsenoside Rg1 (derived from ginseng root) has been found to have many vasoprotective activities. The present study was undertaken to examine effect of ginsenoside Rg1 on the secretion of nitric oxide (NO) in human umbilical vein endothelial cells (HUVECs) stimulated with or without tumor necrosis factor-alpha (TNF-alpha). We showed here that ginsenoside Rg1 can increase the basal and TNF-alpha-attenuated NO production in a dose-dependent manner. As little is known regarding the vascular molecular mechanism of ginsenoside Rg1 on HUVECs and proteomic technique has more advantages in molecular identification, we attempted to use proteomic analysis to explain vascular molecular mechanism of ginsenoside Rg1 on HUVECs. Proteomic analytical result showed that 21 protein spots were changed in TNF-alpha stimulated HUVECs, including 9 up-regulated spots, 11 down-regulated spots, and 1 spot detected in TNF-alpha stimulated group only. The expression level of proteins such as MEKK3, phosphoglycerate mutase was increased, and nitric-oxide synthase, mineralocorticoid receptor were decreased in TNF-alpha stimulated HUVECs, while ginsenoside Rg1 could prevent this change or reverse to some degree. This study suggested that NO production increased via ginsenoside Rg1 played an important role in the protective effect on TNF-alpha stimulated HUVECs and was helpful to deeply understand the active mechanism of ginsenoside Rg1 to HUVECs at the molecular level.

Blotting, Western↗
PubMed2006

Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-alpha.

AIM: To investigate the proliferation of vascular smooth muscle cells (VSMC) affected by ginsenoside Rg1 and further explore the molecular mechanism of ginsenoside Rg1 using proteomics. METHODS: The proliferation of VSMC was measured by MTS assay kit and flow cytometry. Proteomic alterations were analyzed using two-dimensional electrophoresis and peptide mass fingerprinting. Differential proteins found in proteomics were confirmed by RT-PCR. RESULTS: The proliferation of VSMC was enhanced significantly after tumor necrosis factor-alpha (TNF-alpha) treatment, and ginsenoside Rg1 treatment inhibited proliferation in a dose-dependent manner. Proteomic analysis showed 24 protein spots were changed, including 17 spots that were increased and 7 spots that were decreased. Ginsenoside Rg1 could restore the expression levels of these proteins, at least partly, to basic levels of untreated cells. The expression of G-protein coupled receptor kinase, protein kinase C (PKC)-zeta, N-ras protein were decreased, while cycle related protein p21 was increased by ginsenoside Rg1 in TNF-alpha treated VSMC. CONCLUSION: PKC-zeta and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC.

Animals↗
PubMed2006

Pharmacokinetics of puerarin and ginsenoside Rg1 of CBN injection and the relation with platelet aggregation in rats.

In order to study the pharmacokinetics of puerarin and ginsenoside Rg1 of cerebral blood nutrition (CBN) and its relationship with pharmacodynamics of platelet aggregation induced by ADP in rat, the blood samples after injection were collected. The concentrations of puerarin and ginsenoside Rg1 in plasma were determined by RP-HPLC, and the platelet aggregations were observed simultaneously. The data showed that there was distinct statistic significance (p < 0.01) for puerarin processing, which was a single compartment model with quick elimination rate (t(1/2beta) = 18 min) and MRT (26 min), while ginsenoside Rg1 processing was a double compartment model with rapid distribution rate (t(1/2alpha) = 8 min), slow elimination rate (t(1/2beta) = 11 hours) and MRT (3.3 hours). Effects of anti-platelet aggregation were presented at 5-10 min, 45-90 min and 6-8 hours after injection separately, and the corresponding concentrations of puerarin were 25-21 microg/ml, 4.5-0.8 microg/ml and 0 microg/ml, ginsenoside Rg1 were 7.6-6.7 microg/ml, 1.2-0.6 microg/ml and 1.8-0.5 microg/ml. The two components presented a positive correlation between their concentrations and the effect of anti-platelet aggregation in 5-10 min after CBN injection (coefficient of correlation were 0.999 and 0.995). However, it was noted that the effect was still stronger even when concentrations of puerarin and ginsenoside Rg1 in plasma decreased. Therefore, puerarin and ginsenoside Rg1 not only had different pharmacokinetics, but also had a positive correlation with platelet aggregation, just in 5-10 min after CBN injection.

Animals↗
PubMed2002

[Possible mechanisms of the protective effect of ginsenoside Rg1 on apoptosis in substantia nigra neurons].

AIM: To investigate the role of ginsenoside Rg1 in preventing against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced apoptosis of the substantia nigra neurons in the mouse model of Parkinson's disease (PD). METHODS: C57B1 male mice were given MPTP i.p. in the PD model group. Different doses of ginsenoside Rg1 (2.5, 5.0 and 10.0 mg.kg-1) were given i.p. 3 days prior to MPTP in the pretreatment group. Nissl staining, tyrosine hydroxylase (TH) immunostaining and TdT-mediated duTP nick-end labeling (TUNEL) staining were used to observe the damage of nigral neurons. The method of immunostaining was used to detect the caspase-3 activity, expression of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS). RESULTS: Pretreatment with ginsenoside Rg1 was shown to prevent the loss of Nissl staining neurons and TH-positive neurons, and decrease the percent of TUNEL-positive. Simultaneously, Rg1 was found to reduce caspase-3 activity and the expression of iNOS. CONCLUSION: Ginsenoside Rg1 showed protective effect on MPTP-induced apoptosis in the mouse nigral neurons and this effect may be attributable to reducing the expression of iNOS and inhibiting the activation of caspase-3.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2006

Ginsenoside Rg1 inhibits tumor necrosis factor-alpha (TNF-alpha)-induced human arterial smooth muscle cells (HASMCs) proliferation.

In China, the ginseng root began to be used in medicine over 2000 years ago. Ginsenosides are the most important component isolated from ginseng. The aim of this study was to determine the effects of ginsenoside Rg1 on the proliferation and molecular mechanism in cultured human arterial vascular smooth muscle cell (HASMC) induced by tumor necrosis factor-alpha (TNF-alpha). It was shown that ginsenoside Rg1 significantly inhibited TNF-alpha-induced HASMC proliferation in a dose-dependent manner. Treatment with ginsenoside Rg1, which blocked the cell cycle in the G1-phase, induced a downregulation of cyclin D1 and an upregulation in the expression of p53, p21(WAF/CIP1), and p27(KIP1). MEK inhibitors PD98059, U0126, and phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin, but not p38-inhibitor SB203580 or JNK-inhibitor SP600125 significantly aggravated ginsenoside Rg1-inhibited HASMC proliferation. Ginsenoside Rg1 markedly inactivated the extracellular signal-regulated kinases (ERK1/2) and protein kinase B (PKB), indicating that the inhibition of ginsenoside Rg1 on HASMC proliferation was associated with ERK and PI3K/PKB pathways. The inactivation of ERK and PI3K/PKB pathways and modulation of cell-cycle proteins by ginsenoside Rg1 may be of importance in inhibition of HASMCs proliferation.

Cell Line↗
PubMed2004

Ginsenoside Rg1 enhances CD4(+) T-cell activities and modulates Th1/Th2 differentiation.

Panax ginseng is commonly used as a tonic medicine in Asian countries such as Korea, China, and Japan. It has been reported that ginsenoside Rg1 in P. ginseng increases the proportion of T helper (Th) cells among the total number of T cells and promotes IL-2 gene expression in murine splenocytes. This implies that ginsenoside Rg1 increases the immune activity of CD4(+) T cells, however, the exact mechanism remains unknown. The present study elucidated the direct effect of Rg1 on helper T-cell activities and on Th1/Th2 lineage development. The results demonstrated that ginsenoside Rg1 had no mitogenic effects on unstimulated CD4(+) T cells, but augmented CD4(+) T-cell proliferation upon activation with anti-CD3/anti-CD28 antibodies in a dose-dependent manner. Rg1 also enhanced the expression of cell surface protein CD69 on CD4(+) T cells. In Th0 condition, ginsenoside Rg1 increases the expression of IL-2 mRNA, and enhances the expression of IL-4 mRNA on CD4(+) T cells, suggesting that Rg1 prefers to induce Th2 lineage development. In addition, ginsenoside Rg1 increases IL-4 secretion in CD4(+) T cells under Th2 skewed condition, while decreasing IFN-gamma secretion of cells in Th1 polarizing condition. Thus, Rg1 enhances Th2 lineage development from the naïve CD4(+) T cell both by increasing Th2 specific cytokine secretion and by repressing Th1 specific cytokine production. Therefore, these results suggest that ginsenoside Rg1 is a desirable agent for enhancing CD4(+) T-cell activity, as well as the correction of Th1-dominant pathological disorders.

Animals↗
PubMed1993

Ginsenoside Rg1 inhibits the brain cAMP phosphodiesterase activity in young and aged rats.

1. The in vitro effect of ginsenoside Rg1 from Panax ginseng on the low- and high-KM cyclic AMP phosphodiesterase (cAMP PDE) activity in the frontal cortex, striatum, hypothalamus and hippocampus of young (4-5-month old) and aged (22-month old) rats has been studied. 2. Administered in increasing concentrations (from 5 x 10(-5) M up to 5 x 10(-4) M), ginsenoside Rg1 exerted a pronounced inhibitory effect on the low- and high-KM enzyme activity in all brain structures studied in rats of both age groups. 3. Ginsenoside Rg1 exhibited inhibitory potency similar to that of theophylline. 4. The present results provide evidence for the CNS effects of ginsenoside Rg1 through inhibition of the intracellular level of cAMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2004

[Effect of ginsenoside Rg1 on the influence of neprilysin expression induced by LPS in BT325 cell line].

OBJECTIVE: To investigate the effect of ginsenoside Rg1 on the influence of neprilysin expression induced by LPS in BT325 cell line. METHOD: MTT was used to measure the levels of the survival rate of BT325 cultured with ginsenoside Rg1 and LPS in different concentrations. The expression of NEP was measured by RT-PCR. RESULT: The survival rate of BT325 was obviously inhibited by LPS, and the expression of NEP was decreased. The survival rate of BT325 was obviously raised by ginsenoside Rg1, and the expression of NEP was increased. CONCLUSION: LPS can cause cell damage, and decrease the expression of NEP. Ginsenoside Rg1 can exert neuroprotective properties which protects BT325 cell line from the cell toxicity of LPS.

Cell Line, Tumor↗
PubMed2026

Integrated network pharmacology, molecular docking, and experimental validation to reveal the potential mechanism of Ginsenoside Rg1 on chronic obstructive pulmonary disease.

Ginsenoside Rg1 (GS Rg1), a natural flavonoid exhibiting anti-inflammatory and antioxidant properties, holds significant potential for treatment chronic obstructive pulmonary disease (COPD). Nevertheless, the precise mechanisms underlying its therapeutic effects remain to be fully elucidated. This study aimed to explore the role and potential mechanism of GS Rg1 in the treatment of COPD using network pharmacology, molecular docking, and experimental validation.Targets related to GS Rg1 and COPD were screened from public databases, and the potential common targets were then imported into the STRING database to construct a protein-protein interaction (PPI) network. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis were performed to identify key signaling pathways.&#xa0;Molecular docking was employed to predict the binding interactions between GS Rg1 and core targets. A BEAS-2B cell model induced by lipopolysaccharide(LPS) and cigarette smoke extract(CSE) was used to explore the protective mechanisms of GS Rg1. Western blot analysis was conducted to validate the critical targets and pathways involved in the anti-COPD effects of GS Rg1. Network pharmacology analysis revealed 105 common targets between GS Rg1 and COPD.&#xa0;The EGFR/PI3K/AKT and EGFR/STAT3 signaling pathways were selected for further validation. GS Rg1 was demonstrated to effectively inhibit inflammation and mucus hypersecretion in vitro models of COPD. Western blot results showed that GS Rg1 treatment significantly downregulated the expression of proteins involved in the EGFR/PI3K/AKT and EGFR/STAT3 signaling pathway, consistent with the network pharmacology findings. CSE/LPS exposure induces inflammation and oxidative stress in COPD by disrupting the EGFR/PI3K/AKT and EGFR/STAT3 signaling pathways, and GS Rg1 significantly alleviates these effects, which may be partially through regulating the EGFR/PI3K/AKT and EGFR/STAT3 signaling pathway.

Ginsenosides↗
PubMed2005

[Effect of ginsenoside Rg1 on neprilysin expression induced by LPS in SK-N-SH cell line].

OBJECTIVE: To investigate the effect of ginsenoside Rg1 on the neprilysin (NeP) expression induced by LPS in SK-N-SH cell line. METHODS: MTT was used to measure the survival rate of SK-N-SH cultured with ginsenoside Rg1 at different concentrations (5, 10, 20 micromol/L) and LPS (50 mg/L). The expression of NEP was measured by RT-PCR. RESULT: The survival rate of SK-N-SH was obviously inhibited by LPS, the expression of NEP was decreased. On the other hand, the above alteration induced by LPS was reversed by ginsenoside Rg1. CONCLUSION: This study demonstrates that LPS can cause cell damage and the decrease of NEP expression. Ginsenoside Rg1 can protect SK-N-SH cells against the injury induced by LPS, increase NEP expression.

Cell Line, Tumor↗
PubMed1997

[Study on the anti-apoptotic mechanism of ginsenoside Rg1 in cultured cortical neurons].

Ginsenoside Rg1 is an active principle isolated from Panax ginseng CA Meyer. Primary neuronal culture was performed with different concentrations of Rg1. On the 14th day, the culture was changed to serum-free medium. On the 16th day, neurons were harvested and assayed under microscope and fluorescence microscope. The result showed that serum withdrawal from the medium induced apoptosis in primary cultured cortical neurons. Rg1 (1, 10 mumol.L-1) was shown to inhibit apoptosis and protect neurons against injury. Membrane fluidity was measured using fluorescence spectrophotometer in five groups of cultured cortical neurons: control (complete medium), apoptosis (serum-free medium), Rg1 0.1 mumol.L-1, Rg1 1 mumol.L-1 and Rg1 10 mumol.L-1. Neurons were isolated enzymatically and loaded with the fluorescent dye, DPH (1, 6-diphenyl-1,3,5-hexatriene). Membrane fluidity in control neurons (eta 1.2928 +/- 0.1426) was shown to be significantly higher than that in apoptosis cells (eta 2.9277 +/- 0.2004). The membrane fluidity of neurons treated with Rg1 (0.1, 1, 10 mumol.L-1) increased significantly (eta 2.9172 +/- 0.1604, 2.4731 +/- 0.2187, 1.6436 +/- 0.1483). These findings indicate a substantial alteration of membrane fluidity with neuronal apoptosis. Increment of membrane fluidity provides an aspect of elucidating the mechanism of Rg1's anti-apoptosis function.

Animals↗
PubMed2006

[Effect of absorption enhancers on nasal ginsenoside Rg1 delivery and its nasal ciliotoxicity].

AIM: The enhancing activity and safety of several absorption enhancers were evaluated as potential nasal absorption enhancers to increase intranasal absorption of ginsenoside Rg1. METHODS: Nasal circulatory perfusion test in vivo had been employed to investigate the effect of absorption enhancers for nasal mucosa absorption of ginsenoside Rgl in rats. The safety of the absorption enhancers were evaluated by testing cilia movement of the in situ toad palate model, the hemolysis of erythrocyte membrane of the rabbit, leaching of protein and LDH from the mice nasal mucosa and the effect on cilia structural and specific cellular changes of nasal mucosa. RESULTS: Absorption enhancers were necessary to facilitate ginsenoside Rg1 absorption by nasal mucosa. Among the absorption enhancers 1% sodium deoxycholate had great effect to facilite ginsenoside Rgl absorption by nasal mucosa; 1% dipotassium glycyrrhizinate and 1% azone had moderate effect to facilitate ginsenoside Rg1 absorption by nasal mucosa; 1% Tween-80, 2% beta-cyclodextrin, 0.5% borneol (dissolved in paraffin liquid), 0.5% chitosan, 5% hydroxypropyl-beta-cyclodextrin and 0.1% EDTA had low effect to facilitate ginsenoside Rgl absorption by nasal mucosa. 1% sodium deoxycholate, 1% azone and 1% dipotassium glycyrrhizinate had serious nasal toxicity; 1% Tween-80, 2% beta-cyclodextrin, 5% hydroxypropyl-beta-cyclodextrin had moderate nasal toxicity; 0.5% borneol (dissolved in paraffin liquid), 0.5% chitosan and 0.1% EDTA have little nasal toxicity. CONCLUSION: 0.5% borneol and 0.5% chitosan were the promising candidates having a good balance between enhancing activity and safety for nasal ginsenoside Rg1 delivery.

Absorption↗