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At least 19 recordsLinked to original sources
PubMed1978

Stimulatory effect of ginsenosides on DNA, protein and lipid synthesis in rat bone marrow and participation of cyclic nucleotides.

Effects of several kinds of ginsenosides, saponins from Panax ginseng on DNA, RNA, protein and lipid synthesis in bone marrow were investigated. Single i.p. injection of 0.5--1 mg/100 g body weight of ginsenosides Rb2, Rc, Re and Rg1 4 h prior to the sacrifice increased DNA synthesis in bone marrow cells. RNA, protein and lipid synthesis were also increased. The direct addition of ginsenosides Rb1, Rb2 and Rc mixture (GNS) enhanced DNA synthesis. Cyclic AMP levels in bone marrow cells were decreased 20 min after i.p. injection of ginsenosides Rb2, Rc and Rg1 and the direct addition of ginsenosides Rb2, Rc and Rg1 also decreased cyclic AMP levels. While cyclic GMP levels were increased by administration of ginsenosides Rb2, Re and Rg1. Relationship between chemical structure and actions of ginsenosides and the role of cyclic nucleotides in the stimulatory action of ginsenosides on DNA synthesis in bone marrow cells were discussed.

Animals↗
PubMed2026

Comprehensive Identification of WDR Gene Family in Panax ginseng: PgWDR Gene Expression Analysis with Ginsenosides Biosynthesis Under MeJA.

Panax ginseng (Panax ginseng C.A. Mey.) produces pharmacologically valuable ginsenosides. WD40-repeat (WDR) proteins act as versatile regulators of plant specialized metabolism, yet their biological roles under methyl jasmonate (MeJA) elicitation remain largely uncharacterized in ginseng. In this study, we identified 29 PgWDR family members at the whole-genome level, and systematically analyzed their phylogeny, gene structure, cis-acting promoter elements, as well as organ- and development-dependent expression patterns. Six candidate genes potentially associated with ginsenoside biosynthesis were screened through integrating gene-metabolite correlation analysis and gene co-expression analysis. Under MeJA treatment, three of these candidates showed statistically significant expression responses, while the other three exhibited variable expression fluctuations with no statistical significance. PgWDR24 displayed a positive correlation with key ginsenoside biosynthetic enzyme genes, and a negative correlation with protopanaxadiol-type ginsenoside accumulation. Combined with its predicted nuclear localization, we hypothesize that PgWDR24 participates in the negative modulation of protopanaxadiol-type ginsenoside accumulation, although further genetic functional validation is still required. This work provides valuable candidate genes for deciphering ginsenoside regulatory networks and offers support for molecular-assisted breeding of high-quality ginseng.

Panax ginseng C. A. Mey.↗
PubMed1992

[Protective effects of ginsenosides on warm ischemic damages of the rabbit kidney].

Renal function and morphology were studied before and after 60 min of renal ischemia and contralateral nephrectomy in two groups of rabbits. The animals were pretreated with ginsenosides (n = 22) and saline (n = 22) respectively, the latter as control. Results showed that ginsenosides (30 mg/kg body wt.) pretreatment by intravenous injection 10 min before warm ischemia resulted in the survival of all the animals with better renal function, 1, 3 and 7 days after blood urea nitrogen, fraction of excreted sodium and urine protein were observed in the control rabbits and a less pronounced increase was noted (P less than 0.05) after pretreatment with ginsenosides. The appearance of kidney tissue taken from surviving rabbits with Ginsenosides pretreatment was found to be normal under light microscope. Severe tubular necrosis was observed in kidneys of the control group. Tissues were examined with a transmission electron microscope. ginsenosides have protective effects on the epithelial cells of the proximal convoluted tubules, and microvilli and mitochondria were less damaged by ischemia than those of the control animals. There was also a large amount of ribosome on rough surfaced endoplasmic reticulum in the cells of ginsenosides-treated kidney, reflecting their ability to stimulate ribonucleic acid and protein synthesis. This is considered to be the basis of improvement of renal function.

Acute Kidney Injury↗
PubMed1992

Ginsenosides protect pulmonary vascular endothelium against free radical-induced injury.

We studied the actions of saponin (ginsenosides) from Panax ginseng on free radical-induced pulmonary endothelial injury which is manifest as reversal of the normal vasodilator response to acetylcholine in perfused, vasoconstricted lungs. 50 or 200 micrograms/ml ginsenosides prevented this injury response and also reduced the pulmonary edema which follows free radical injury but did not alter the normal ACh-induced vasodilation in intact lungs. In control perfused lungs preconstricted with U46619, the ginsenoside mixture or purified ginsenosides Rb1 and Rg1 caused vasodilatation. This effect was eliminated by 100 microM nitro-L-arginine, an inhibitor of nitric oxide synthase. In cultured bovine aortic endothelial cells, ginsenosides (10 micrograms/ml) stimulated the conversion of [14C]-L-arginine to [14C]-L-citrulline. These data indicate that GS may cause vasorelaxation and prevent manifestations of oxygen free radical injury by promoting release of nitric oxide.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Effect of ginsenoside Rgl on the release of enzymes by cultured endothelial cells.

The effects of ginsenoside Rgl, isolated from Ginseng Radix, on the secretion of plasminogen activator and angiotensin-converting enzyme from cultured human umbilical vein endothelial cells were investigated in vitro. Ginsenoside Rgl significantly increased the secretion of plasminogen activator from the cells both with and without stimulation of the cells by thrombin. Ginsenoside Rgl also remarkably induced the secretion of angiotensin-converting enzyme from the cells. Furthermore, ginsenoside Rgl showed some morphological alteration in the surface membrane of the cells. In addition, survival-promoting effect of CPAE cell line by ginsenoside Rgl was observed.

Cell Survival↗
PubMed1992

Inhibitory effect of ginsenosides on migration of arterial smooth muscle cells.

Migration of arterial smooth muscle cells (SMC) in the arterial wall plays an important role in the formation of intimal thickening of atherosclerotic lesions. In this study, we examined the effect of ginsenosides on SMC migration induced by platelet-derived growth factor (PDGF) and SMC-derived migration factor (SDMF). Ginsenosides had inhibitory effects on SMC migration and the striking effects were observed with ginsenoside-Rb2 and -Rc in a dose-dependent manner. These results suggest that the administration of ginsenosides on the patients may prevent intimal thickening, in part, by inhibiting SMC migration in the arterial wall.

Animals↗
PubMedDate not supplied

The decline of atrial natriuretic peptide (ANP) gene expression in older rats and the effects of ginsenoside on ANP gene expression.

1. The levels of atrial natriuretic peptide(ANP) gene expression in rat atria at 2-3 and 14-18 months of age and the effects of ginsenosides on r-ANP gene expression by determining the concentration of ANP-mRNA were investigated. The male and female rats were abdominally (i.p.) injected with aqueous solution of ginsenosides prepared from ginseng stems and leaves (G-PSL) and ginseng roots (G-PR), 50 mg/kg body wt, once a day for 7 days. Atria total RNA was extracted by the cold phenol method. The ANP-mRNA contents were determined using the Northern blot and dot blot hybridization technique with alpha-32*P-labelled r-prepro-ANP-cDNA probe. 2. The ANP-mRNA contents of 14-18 month rats were remarkably less than that of 2-3 month rats. The levels of male and female rats' atria at 14-18 months were about 15 and 60%, the content of male and female rats at 2-3 months respectively. 3. G-PSL and G-PR increased the ANP-mRNA content of male rats at 14-18 months 1- and 2-fold, respectively, whereas G-PSL and G-PR decreased the ANP-mRNA content in male rats of age 2-3 months. 4. These results revealed that the ANP gene expression declined during ontogenic ageing development and ginsenosides possessed anti-ageing effects in the heart endocrineous function aspect.

Aging↗
PubMed2026

Direct targeting of ORAI1 by ginsenoside Rg3 modulates calcium signaling and senescence-associated AMPK-NRF2 activation.

BACKGROUND: 20(S)-ginsenoside Rg3 (Rg3(S)), a major saponin derived from red ginseng, exhibits diverse biological activities, including antioxidant and anti-senescence effects. However, the direct molecular targets through which Rg3(S) regulates calcium signaling and its role at membrane contact sites during cellular senescence remain largely unknown. METHODS: Plasma membrane (PM)-endoplasmic reticulum (ER) contacts and related protein interactions were analyzed using proximity ligation assays and co-immunoprecipitation. Direct binding of Rg3(S) to ORAI1 was validated using cellular thermal shift assays and microscale thermophoresis. Molecular docking simulations followed by site-directed mutagenesis were used to define critical binding residues. Cytosolic calcium levels and cellular senescence were assessed using calcium imaging and senescence-associated β-galactosidase staining. RESULTS: Rg3(S) increased cytosolic calcium levels independently of ER calcium depletion and was accompanied by a reduction in PM-ER contacts. Rg3(S) directly bound to ORAI1 in a dose-dependent manner, identifying ORAI1 as a previously unrecognized molecular target of ginsenoside Rg3. Molecular docking revealed LYS204 and ILE229 within the extracellular loop of ORAI1 as key residues maintaining this interaction. Mutation of these residues abolished Rg3(S)-induced calcium influx, leading to impaired activation of the AMPK-NRF2 pathway and attenuation of the anti-senescence effect of Rg3(S). CONCLUSION: These findings identify ORAI1 as a key molecular mediator of ginsenoside Rg3(S)-induced calcium signaling linked to cellular senescence. By modulating PM-ER contact sites and cytosolic calcium dynamics, Rg3(S) attenuates senescence, providing new mechanistic insight into the anti-aging potential of ginseng-derived compounds beyond autophagy-centered pathways.

Calcium signaling↗
PubMed2026

Alleviation of Helicobacter pylori-Induced Pathogenicity and Gastric Inflammation by Majonoside-R2- and Ginsenoside Rg1-Rich Fractions From Panax vietnamensis Ha Et Grushv.: A Metabolomics-Guided Investigation.

Helicobacter pylori infection remains a major global health concern due to its association with gastric inflammation, ulceration, and gastric malignancies. This study evaluated the effects of Ngoc Linh ginseng (Panax vietnamensis Ha et Grushv.) root fractions on H. pylori virulence and host inflammatory responses. UHPLC-MS/MS-based metabolomic profiling coupled with feature-based molecular networking was employed to characterize the chemical profiles of different solvent fractions, identifying the dichloromethane (DCM) fraction as enriched in ginsenosides, particularly the ocotillol-type saponin majonoside R2 (MR2). In vitro assays showed that, despite minimal direct antibacterial activity, the DCM fraction at sub-inhibitory concentrations significantly reduced urease activity, acid tolerance, biofilm formation, and the expression of major virulence genes, including vacA and cagA. In H. pylori-infected AGS gastric epithelial cells, the DCM fraction and MR2 decreased VacA and CagA translocation, suppressed pro-inflammatory signaling and cytokine production, restored antioxidant defenses, and alleviated mitochondrial apoptosis. By contrast, ginsenoside Rg1 selectively modulated host inflammatory and oxidative stress responses without affecting bacterial virulence gene expression. These results demonstrate that Ngoc Linh ginseng root fractions mitigate H. pylori-induced pathogenic effects primarily through anti-virulence and host-directed mechanisms, highlighting their potential relevance for the development of gastric health-promoting functional products.

Helicobacter pylori↗
PubMed1992

Studies on absorption, distribution, excretion and metabolism of ginseng saponins. VIII. Isotope labeling of ginsenoside Rb2.

To clarify the pharmacokinetics of absorption, distribution and excretion of ginsenoside Rb2 (Rb2), one of the major saponins of the root of Panax ginseng, following oral administration to rats, a tritium (3H) labeling of Rb2 was examined. The C-12 position of Rb2 was labeled with 3H-sodium borohydride (3H-NaBH4) and 12-3H Rb2 and 12-3H-epi Rb2 was synthesized. This method of specific position labeling of Rb2 may be applicable to other ginsenosides. In the near future, the pharmacokinetics of Rb2 in rats may be clarified with 3H labeled Rb2.

Animals↗
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. 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. 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↗
PubMed1992

Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings.

The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve terminals, but was associated with an increase in uptake of the precursor choline. In the present studies, analysis of choline uptake kinetics indicated that Rb1 increased the maximum velocity of choline uptake, while the affinity of the choline uptake carrier for choline (Km) was not significantly altered. Acute treatment with Rb1 did not alter the number of [3H]hemicholinium-3 (HC-3) binding sites in any of three cholinergic brain regions examined, suggesting that the increase in the maximum velocity of choline uptake was not associated with an increase in the number of choline carriers. However, chronic (3 day) administration of Rb1 did increase the number of choline uptake sites in the hippocampus, and to a lesser extent in the cortex.

Acetylcholine↗
PubMed2024

Dissecting the anti-obesity components of ginseng: How ginseng polysaccharides and ginsenosides target gut microbiota to suppress high-fat diet-induced obesity.

INTRODUCTION: Ginseng demonstrates therapeutic potential in treating obesity, with both experimental and clinical studies suggesting its anti-obesity effects are mediated by gut microbiota. Nonetheless, the specific chemical components responsible for this effect remain largely unidentified. OBJECTIVES: This study aims to investigate the anti-obesity effects and mechanisms of ginseng polysaccharides (GP) and ginsenosides (GS), the primary chemical components of ginseng, with a focus on their impact on gut microbiota. METHODS: The impact of GP and GS on high-fat diet (HFD)-induced obesity was assessed using a mouse model. Molecular mechanisms were explored through a combination of chemical analysis, metagenomics, RT-qPCR, ELISA, and biochemical assays. RESULTS: GP or GS administration effectively prevented adiposity in HFD-fed mice, and both effects were mediated by gut microbiota. Chemical analysis revealed diverse glycosyl groups in GP and GS. Metagenomics data suggested that GP-enriched species, e.g., Bacteroides stercorirosoris and Clostridiales bacterium encoded carbohydrate-active enzymes GH35, GH43 and PL9_1, while GS-enriched Sulfurospirillum halorespirans encoded GH16_5. These enzymes facilitated the utilization of glycosyl groups in GP and GS, selectively stimulating bacterial growth and reshaping the gut microbiota. Furthermore, bacterial species enriched by GP or GS encoded specific functional genes involved in short-chain fatty acid (SCFA) synthesis (K00625 and K00925 for GP; K18118, K00100, and K18122 for GS) and intestinal gluconeogenesis (IGN) (K01678, K00024, and K01596 for GP; K18118 and K00278 for GS). Consequently, the SCFA-GLP-1/PYY signaling and IGN were activated by both GP and GS to ameliorate obesity phenotypes. CONCLUSION: GP and GS, containing diverse glycosyl groups, selectively stimulate specific gut bacteria, triggering mechanisms involved in SCFA-GLP-1/PYY signaling and IGN activation to reduce adiposity in HFD-fed mice. The study enhances understanding of the chemical components crucial for the gut microbiota-mediated anti-obesity effect of ginseng. The mechanistic understanding provides valuable insights for developing ginseng-based drugs or health products to combat obesity.

Gastrointestinal Microbiome↗
PubMed1992

Studies on the enzyme immunoassay of bio-active constituents in oriental medicinal drugs. VI. Enzyme immunoassay of ginsenoside Rb1 from Panax ginseng.

Enzyme immunoassay (EIA) of ginsenoside Rb1 (GRb1), one of the glucosides of protopanaxadiol from Panax ginseng, was explored. A carrier protein (bovine serum albumin (BSA)) was coupled to the C-26 position on the unsaturated side chain of the protopanaxadiol moiety to prepare the immunogen. In order to perform bridge heterologous EIA, a label (beta-D-galactosidase) was introduced at C-26 of the saturated side chain to obtain labeled antigen. Anti-GRb1 antisera were elicited in rabbits by immunization with GRb1-BSA conjugate (9). The double antibody method (with goat anti-rabbit IgG antiserum) was used to separate the bound and free GRb1-beta-Gal. A satisfactory standard curve for EIA of GRb1 was obtained in the range of 0.04-10 ng/tube. In a comparison of the assay results obtained by EIA and HPLC, the linear regression equation and correlation coefficient for the two methods were y (EIA) = 9.18x(HPLC)-0.033 and 0.98, respectively. The anti-GRb1 antiserum cross-reacted with GRb2 (21.8%) and GRc (10.6%), which are also constituents of Panax ginseng.

Animals↗
PubMed1992

[Protection on experimental sinus node dysfunction in rabbits with ginsenosides].

This experiment was carried out to evaluate the effect of ginsenosides from stems and leaves (GSL) on the sinus node dysfunction (SND) by observing the changes of the electrophysiological parameters of sinus node in limited period. Anesthetized rabbits were randomly divided into 3 groups. In the acute experiment, GSL, 50 mg/kg, iv, was given to the GSL group (G), n = 12. Normal saline (NS), the same volume, to the control group (C), n = 12. After GSL was administered 30-50 mg/kg.d for 14 days, iv, another data were obtained from chronic experimental group (CE), n = 15. The results show that the parameters, spontaneous cycle length (SCL), maximal sinus node recovery time (SNRTmax), corrected sinus node recovery time (CSNRT) were shorter in G group and CE group than C group respectively (P less than 0.05, P less than 0.01). It was suggested that GSL exerted protective effects on the experimental sinus node dysfunction.

Animals↗
PubMed1992

[In vitro and in vivo effects of ginsenoside Rh2 on the proliferation of serous cystadenocarcinoma of the human ovary].

Inhibition of human ovarian cancer cell proliferation in vitro and in vivo by Ginsenoside Rh2(Rh2) isolated from Red Ginseng was examined by using a cell line (HRA) derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HRA cell proliferation in vitro was inhibited in a dose-dependent manner with between 10 and 100 microM of Rh2. The uptake of radiolabeled precursors (3H-thymidine, 3H-uridine, and 3H-varine) by HRA cells was also inhibited in a dose-dependent manner with between 30 and 100 microM of Rh2. The growth of HRA cells transplanted into nude mice was not significantly inhibited by Rh2 alone. On the other hand, when cisplatin was administered together with 10 microM, 30 microM, or 50 microM Rh2, the growth of HRA cells was inhibited 31 and 35 days after tumor inoculation. Survival was also prolonged when cisplatin was administered with 10 microM and 30 microM Rh2. These results suggest that there is a synergistic effect between cisplatin and Rh2.

Animals↗
PubMed1977

Potentiation of the NGF-mediated nerve fiber outgrowth by ginsenoside Rb1 in organ cultures of chicken dorsal root ganglia.

The fiber outgrowth induced by ACh, dibutyryl cyclic AMP and dibutyryl cyclic GMP in explanted chick embryonic dorsal root ganglia differed distinctly from that be nerve growth factor (NGF) and submandibular gland extract of adult male mice. Ginsenoside Rb1 potentiated the effects of NGF and submandibular extract at concentrations of 3 and 30 muM, but did not potentiate the effects of ACh, dibutyryl cyclic AMP and dibutyryl cyclic GMP. NGF-antibody inhibited the effects of NGF, but not the effects of ACh, dibutyryl cyclic AMP and dibutyryl cyclic GMP, Concanavalin A and KCL did not promote fiber outgrowth.

Acetylcholine↗