20(S)-Ginsenoside Rg3 is the main component of Red ginseng. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.
IC50 Target
p65
;
COX-2
;
Human Endogenous Metabolite
;
Na+ channel
32.2 mu;M (IC50)
hKv1.4 channel
32.6 mu;M (IC50)
Aβ40
;
Aβ42
;
体外研究 (In Vitro)
Ginsenoside Rg3 plays an important role in its effect on the Na+ channel. Treatment with Ginsenoside Rg3 reversibly inhibits the inward Na+ peak current (INa) with an IC50 of 32.2±4.5 μM, and the inhibition is voltage-dependent[1]. Ginsenoside Rg3 at 100 μM inhibits the hKv1.4 channel currents by an average of 65%.The Ginsenoside Rg3 effect is concentration-dependent and reversible. The IC50 value and Hill coefficient are 32.6±2.2 μM and 1.59±0.13, respectively[2]. Ginsenoside Rg3 shows the significant inhibition of NF-κB activity thereby reduced COX-2 expression. To examine the cytotoxicity of Ginsenoside Rg3 on IL-1β-induced inflamed A549 cells, the cells are firstly treated with IL-1β (10 ng/mL) for 4 h and treated with 100 to 900 ng/mL concentration of Ginsenoside Rg3 for 12 h. Cell viability is analyzed using an MTT assay. There is no observed cytotoxicity of Ginsenoside Rg3 in IL-1β-induced inflamed A549 cells compared to only PBS-treated cells (Con).To obtain the anti-inflammatory effects of Ginsenoside Rg3 on inflammation induced human lung epithelial cells, A549 cells inflammation is induced by IL-1β (10 ng/mL) and then treated by 5 μM of Dexamethasone (Dex) or 900 nM of Rg3. The NF-κB activation is analyzed by a western blot analysis to evaluate the effect of Ginsenoside Rg3 treatment on A549 cells. Phospho-NF-κB p65/total NF-κB p65 densitometry in the cells treated with Rg3 shows the significant decrease compared to IL-1β-induced inflamed A549 cells. The meaning of reducing the ratio of p-p65/p65 by Rg3 treatment is associated with NF-κB activation. Ginsenoside Rg3 also downregulates the expression of COX-2 effectively[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Rg3 ((20S)-Rg3) is an Aβ-lowering Natural Compound. APP/PS1 mice are treated with Ginsenoside Rg3 once a day for 4 weeks by intraperitoneal injection (10 mg/kg/day). Aβ ELISA analysis of brain tissues reveal that Ginsenoside Rg3 treatment results in a significant reduction of Aβ40 and Aβ42 in the brain[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
785.01
Formula
C42H72O13
CAS 号
14197-60-5
中文名称
20(S)-人参皂苷 Rg3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Kim JH, et al. A role for the carbohydrate portion of ginsenoside Rg3 in Na+ channel inhibition. Mol Cells. 2005 Feb 28;19(1):137-42.
[2]. Lee JH, et al. Ginsenoside Rg3 inhibits human Kv1.4 channel currents by interacting with the Lys531 residue. Mol Pharmacol. 2008 Mar;73(3):619-26.
[3]. Lee IS, et al. Anti-Inflammatory Effects of Ginsenoside Rg3 via NF-κB Pathway in A549 Cells and Human Asthmatic Lung Tissue. J Immunol Res. 2016;2016:7521601.
[4]. Kang MS, et al. Modulation of lipid kinase PI4KIIα activity and lipid raft association of presenilin 1 underlies γ-secretase inhibition by ginsenoside (20S)-Rg3. J Biol Chem. 2013 Jul 19;288(29):20868-82.
Cell Assay [3]
MTT assays are performed to evaluate the cytotoxicity of Ginsenoside Rg3 on inflamed cells. Ten thousands of A549 cells cultured each well of 96-well plate and are incubated at 37°C and 5% CO2 overnight. After serum starvation using DMEM low glucose without FBS, the medium is changed into RPMI containing IL-1β (10 ng/mL) and the cells are incubated at 37°C and 5% CO2 for 4 h. After 4 h incubation, the cells are treated with Ginsenoside Rg3 (100-900 nM) for 12 h. Thirty microliters of MTT solution (5 mg/mL) is added to each well and the cells are incubated for 2 h. After 2 h incubation in cell culture incubator, the medium containing MTT solution of each well is removed and 50 μL of DMSO is added. Using an automated spectrophotometric plate reader at 570 nm, the optical density of formazan is measured[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [4]
Mice[4] The mice used are heterozygous, double transgenic animals expressing both human APP(K670N/M671L) and PS1(M146L) proteins. These Alzheimer disease model mice are age-matched (3 months old) in all experiments with wild-type littermates. Both sets of mice are produced by crossing heterozygous APP mice with heterozygous PS1 mice and are weaned at 3 weeks and genotyped by PCR of digested tail samples. Ginsenoside Rg3 is prepared in a saline solution containing 0.01% DMSO at a concentration of 10 mg/kg of body weight. Ginsenoside Rg3 (or saline with 0.01% DMSO for controls) is administered daily via intraperitoneal injection. After sacrifice, one hemibrain from each mouse is frozen on dry ice, homogenized in sucrose buffer, and extracted via formic acid for Aβ quantification using a commercial sandwich ELISA kit.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Kim JH, et al. A role for the carbohydrate portion of ginsenoside Rg3 in Na+ channel inhibition. Mol Cells. 2005 Feb 28;19(1):137-42.
[2]. Lee JH, et al. Ginsenoside Rg3 inhibits human Kv1.4 channel currents by interacting with the Lys531 residue. Mol Pharmacol. 2008 Mar;73(3):619-26.
[3]. Lee IS, et al. Anti-Inflammatory Effects of Ginsenoside Rg3 via NF-κB Pathway in A549 Cells and Human Asthmatic Lung Tissue. J Immunol Res. 2016;2016:7521601.
[4]. Kang MS, et al. Modulation of lipid kinase PI4KIIα activity and lipid raft association of presenilin 1 underlies γ-secretase inhibition by ginsenoside (20S)-Rg3. J Biol Chem. 2013 Jul 19;288(29):20868-82.
Ginsenoside Rg1 is one of the major active components of ginseng. Ginsenoside Rg1 ameliorates the impaired cognitive function, displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.
IC50 Target[1][2]
Aβ1-42
;
p65
;
体外研究 (In Vitro)
Ginsenoside Rg1 promotes the proliferation and differentiation of human dental pulp cells (hDPCs). The proliferative ability of hDPCs in Ginsenoside Rg1 is significantly enhanced (p<0.05), especially in the Ginsenoside Rg1 (5 μM) group. ALP activity and gene expressions of DSPP and DMP1 are increased in the induction group, Ginsenoside Rg1 group, and their combination group compared with the control group (p<0.05)[3]. In the RAW264.7 cells stimulated by lipopolysaccharides (LPS) , the level of p-IκBα and p-p65 is significantly higher than in controls and PPAR-γ levels are significantly lower. Treatment with Rg1 vitro inhibits IκBα phosphorylation, reduces NF-κB nuclear translocation and upregulates PPAR-γ expression[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
In the inflamed joints of adjuvant-induced arthritis (AIA) rats, the level of p-IκBα and p-p65 is significantly higher than in controls and PPAR-γ levels are significantly lower. Treatment with Ginsenoside Rg1 in vivo inhibits IκBα phosphorylation, reduces NF-κB nuclear translocation and upregulates PPAR-γ expression[2]. Ginsenoside Rg1 (G-Rg1) and Ginsenoside Rg2 (G-Rg2) reduce the escape latencies on the last two training days compared to the Alzheimer’s disease (AD) model group (p<0.05). In the spatial exploration test, the total time spent in the target quadrant and the number of mice that exactly crossed the previous position of the platform are clearly shorter and lower, respectively, in the AD model group mice than in the normal control group mice (p<0.01), a trend that is reversed by treatment with Ginsenoside Rg1 and Ginsenoside Rg2 (Ginsenoside Rg1, p<0.01; Ginsenoside Rg2, p<0.05). Treatment with Ginsenoside Rg1 and Ginsenoside Rg2 effectively improve cognitive function of the mice that have declined due to AD. Ginsenoside Rg1 and Ginsenoside Rg2 reduce Aβ1-42 accumulation in APP/PS1 mice. In the Ginsenoside Rg1 and Ginsenoside Rg2 treated mice, the pathological abnormalities observed in the APP/PS1 mice are gradually ameliorated. Clear nucleoli and light brown, sparsely scattered Aβ deposits are visible[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
801.01
Formula
C42H72O14
CAS 号
22427-39-0
中文名称
人参皂苷 Rg1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Li N, et al. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer’s disease. J Ginseng Res. 2016 Jan;40(1):9-17.
[2]. Wang P, et al. Effect of ginsenoside Rg1 on proliferation and differentiation of human dental pulp cells in vitro. Aust Dent J. 2012 Jun;57(2):157-65.
[3]. Zhang L, et al. Ginsenoside Rg1 attenuates adjuvant-induced arthritis in rats via modulation of PPAR-γ/NF-κB signal pathway. Oncotarget. 2017 Jul 24;8(33):55384-55393.
Cell Assay [3]
hDPCs are incubated with different concentrations of Ginsenoside Rg1 (0.1, 0.5, 2.5, 5, 10 and 20 μM) . The effects of Ginsenoside Rg1 on the proliferative ability of hDPCs are evaluated by a fibroblast colony forming test, MTT assay and flow cytometry for cell cycle. The control group, osteogenic induction group, Ginsenoside Rg1 (5 μM) group and combination group are designed, and alkaline phosphatase (ALP) activity and FQ-PCR for gene expressions of dentine sialophosphoprotein (DSPP) and dentine matrix protein 1 (DMP1) are performed to evaluate the differentiation of hDPCs[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Mice[1] Male APP/PS1 mice, weighing 20±2 g, and male C57BL/6J mice, weighing 20±2 g, are used. The animals are maintained in an air-conditioned animal center at 23±2°C and a relative humidity of 50±10%, with a natural light-dark cycle. Food and water are available ad libitum. After acclimatization for 1 wk, the mice are divided into four groups (n=10 in each group): the normal control group, the AD model group, the Ginsenoside Rg1 group, and the Ginsenoside Rg2 group. According to the concentration-response curves, the mice in the Ginsenoside Rg1 and Ginsenoside Rg2 groups are injected intraperitoneally once daily with Ginsenoside Rg1 and Ginsenoside Rg2 (30 mg/kg), respectively, dissolved in saline. The mice in the AD model group (APP/PS1 mice) and the normal control group (C57BL/6J nontransgenic littermates) are treated with isodose saline (0.9% w/v). All mice are treated for 1 mo before brain metabolite profiling.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Li N, et al. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer’s disease. J Ginseng Res. 2016 Jan;40(1):9-17.
[2]. Wang P, et al. Effect of ginsenoside Rg1 on proliferation and differentiation of human dental pulp cells in vitro. Aust Dent J. 2012 Jun;57(2):157-65.
[3]. Zhang L, et al. Ginsenoside Rg1 attenuates adjuvant-induced arthritis in rats via modulation of PPAR-γ/NF-κB signal pathway. Oncotarget. 2017 Jul 24;8(33):55384-55393.
(20R)-ginsenoside Rg3 ((20R)-Propanaxadiol), one of the active compounds present in ginseng root, inhibits vascular endothelial growth factor (VEGF)(IC50=10 nM) and antitumor activities[1][2].
分子量
785.01
Formula
C42H72O13
CAS 号
38243-03-7
中文名称
(20R)-人参皂苷Rg3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Liu L, et al. Enzymatic preparation of 20(S, R)-protopanaxadiol by transformation of 20(S, R)-Rg3 from blackginseng. Phytochemistry. 2010 Sep;71(13):1514-20.
[2]. Yue PY, et al. The angiosuppressive effects of 20(R)- ginsenoside Rg3. Biochem Pharmacol. 2006 Aug 14;72(4):437-45.
Ginsenoside Rg6 inhibits TNF-α-induced NF-κB transcriptional activity with an IC50 of 29.34 μM in HepG2 cells. Ginsenoside Rg6 also exhibits apoptosis-inducing effect.
IC50 Target[1][2]
NF-κB
25.12 mu;M (IC50, in SK-Hep1 cell)
NF-κB
29.34 mu;M (IC50, in HepG2 cell)
Apoptosis
;
体外研究 (In Vitro)
Ginsenoside Rg6 inhibits TNF-α-induced NF-κB transcriptional activity with an IC50 of 25.12±1.04 μM in SK-Hep1 cells, consistent with the data from HepG2 cells[1]. Ginsenoside Rg6 exhibits obvious anti-proliferative and apoptosis-inducing effects when it is applied to JK cells in vitro. Ginsenoside Rg6 blocks S arrest in the cell cycle. CCK-8 method shows that after Ginsenoside Rg6 is used, several groups with different concentrations obviously inhibits JK cell proliferation in human lymphocytoma, with evident dose dependency. Based on IC50, the median inhibitory concentration of Ginsenoside Rg6 is 83.08 μM[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
767.00
Formula
C42H70O12
CAS 号
147419-93-0
中文名称
人参皂苷 Rg6
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Cho K, et al. Inhibition of TNF-α-Mediated NF-κB Transcriptional Activity by Dammarane-Type Ginsenosidesfrom Steamed Flower Buds of Panax ginseng in HepG2 and SK-Hep1 Cells. Biomol Ther (Seoul). 2014 Jan;22(1):55-61.
[2]. Chen B, et al. Apoptosis-inducing effect of ginsenoside Rg6 on human lymphocytoma JK cells. Molecules. 2013 Jul 9;18(7):8109-19.
Cell Assay [1]
HepG2 and SK-Hep1 cells are maintained in Dulbecco’s modified Eagle’s medium containing 10% heat-inactivated fetal bovine serum, 100 units/mL Penicillin, and 10 μg/mL Streptomycin, at 37°C and 5% CO2. Cell-Counting Kit (CCK)-8is used to analyze the effect of compounds (e.g., Ginsenoside Rg6; 0.01, 0.1, 1 and 10 μM) on cell toxicity. Cells are cultured overnight in 96-well plate (~1×104 cells/well). Cell toxicity is assessed after the addition of compounds on dose-dependent manner. After 24 h of treatment, 10 μL of the CCK-8 solution is added to triplicate wells, and incubated for 1 h. Absorbance is measured at 450 nm to determine viable cell numbers in wells[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Cho K, et al. Inhibition of TNF-α-Mediated NF-κB Transcriptional Activity by Dammarane-Type Ginsenosidesfrom Steamed Flower Buds of Panax ginseng in HepG2 and SK-Hep1 Cells. Biomol Ther (Seoul). 2014 Jan;22(1):55-61.
[2]. Chen B, et al. Apoptosis-inducing effect of ginsenoside Rg6 on human lymphocytoma JK cells. Molecules. 2013 Jul 9;18(7):8109-19.
Ginsenoside Rg5 is the main component of Red ginseng. Ginsenoside blocks binding of IGF-1 to its receptor with an IC50 of ~90 nM. Ginsenoside Rg5 also inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65.
IC50 Target[1][2]
p65
;
COX-2
;
IGF-1R
90 nM (IC50)
体外研究 (In Vitro)
Ginsenoside Rg5 plays a novel role as an IGF-1R agonist. Ginsenoside Rg5 binds to IGF-1R with an IC50 value of ~90 and its angiogenic activity is inhibited by IGF-1R knockdown. To investigate the possible interaction of Ginsenoside Rg5 with IGF-1R, a docking analysis is performed. Docking results show that Ginsenoside Rg5 binds strongly at two sites, A and B, with Kd values of 20 and 27 nM, respectively, to the cysteine-rich domain of IGF-1R. Pretreatment with Rg5 blocks the binding of radiolabeled IGF-1 to HUVECs with an IC50 value of ~90 μM, which is greater than an IC50 value of ~1.4 nM for unlabeled IGF-1[1]. The results from MTT assay show that MCF-7 cell proliferation is inhibited by Ginsenoside Rg5 treatment for 24, 48 and 72 h in a dose-dependent manner. Ginsenoside Rg5 at different concentrations (0, 25, 50 and 100 μM), induce cell cycle arrest in G0/G1 phase through regulation of cell cycle-related proteins in MCF-7 cells[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Rg5 inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65 in lipopolysaccharides (LPS)-stimulated BV2 microglial cells. Rg5 pretreated group mice show declined expression of NF-κB p65 and COX-2. In the group treated with low dose of Ginsenoside Rg5 (10 mg/kg), there is remarkable tubular damage and infiltration of inflammatory cells. However, at the higher dose of Ginsenoside Rg5 (20 mg/kg), tubules markedly appeare histologically normal and no inflammation and cast formation is observed in kidney tissues[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
767.00
Formula
C42H70O12
CAS 号
186763-78-0
中文名称
人参皂甙 Rg5
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Cho YL, et al. Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation. J Biol Chem. 2015 Jan 2;290(1):467-77.
[2]. Li W, et al. Ginsenoside Rg5 Ameliorates Cisplatin-Induced Nephrotoxicity in Mice through Inhibition of Inflammation, Oxidative Stress, and Apoptosis. Nutrients. 2016 Sep 13;8(9). pii: E566.
[3]. Kim SJ, et al. Anti-breast cancer activity of Fine Black ginseng (Panax ginseng Meyer) and ginsenoside Rg5. J Ginseng Res. 2015 Apr;39(2):125-34.
Kinase Assay [1]
HUVECs are cultured in 24-well plates overnight. The cells are changed to serum-free M199 and incubated for 1 h. The medium is removed, and cells are incubated with fresh serum-free medium containing 0.1 μM-50 mM Ginsenoside Rg5 at 37°C for 20 min followed by the addition of 50 μL (1 μCi) of [125I]IGF-1 and then further incubated for 10 min. The medium is decanted, and cell plates are washed twice with serum-free medium. Cells are lysed in 300 μL of 0.1 N NaOH solution containing 0.1% SDS, transferred to scintillation vials, and mixed with 1 mL of Ultima Gold mixture solution. Cell-associated [125I]IGF-1 is analyzed in a scintillation counter. The nonspecific binding is determined by coincubation with unlabeled IGF-1 (50 nM)[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [3]
MCF-7 (HER2–/ER+) and MDA-MB-453 (HER2+/ER–) human breast cancer cell lines are maintained using RPMI 1640 medium supplemented with 10% (vol/vol) FBS plus 100 units/mL Penicillin and Streptomycin in a 5% carbon dioxide air incubator at 37°C. Cell cytotoxicity is measured by MTT assay. Cells are seeded in 96-well tissue culture plates at the density of 0.2×104 cells per well with 100 μL medium, and are allowed to become attached for 24 h. One hundred microliters of the medium with different concentrations of Ginsenoside Rg5 (e.g., 0 μM, 25 μM, 50 μM, and 100 μM) are added to each well. At indicated times, 30 μL MTT stock solution (3 mg/mL) are added to each well. After culturing the cells at 37°C for 2 h, DMSO is added to dissolve the formazan crystals. The absorbance is read at the wavelength of 540 nm with a microplate reader[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Male ICR mice (6 to 8 weeks old), weighing 25-27 g, are used. After acclimation for one week, mice are randomly assigned into 4 experimental groups with 8 mice in each group: normal control, Cisplatin control, and Cisplatin+Ginsenoside Rg5 groups (10 and 20 mg/kg, respectively). Ginsenoside Rg5 is administered intragastrically at the dose of 10 and 20 mg/kg for 10 days. On the 7th day, animals in Cisplatin control and Ginsenoside Rg5-treated groups receive a single intraperitoneal injection of Cisplatin (25 mg/kg) to induce nephrotoxicity in mice. Mice are anaesthetized with pentobarbital, subsequently sacrificed at 72 h after Cisplatin injection (Day 10). Blood samples are collected and then centrifuged at 3000 rpm to separate the serum and stored at -20 °C for determining blood urea nitrogen (BUN) and creatinine (CRE) levels.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Cho YL, et al. Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation. J Biol Chem. 2015 Jan 2;290(1):467-77.
[2]. Li W, et al. Ginsenoside Rg5 Ameliorates Cisplatin-Induced Nephrotoxicity in Mice through Inhibition of Inflammation, Oxidative Stress, and Apoptosis. Nutrients. 2016 Sep 13;8(9). pii: E566.
[3]. Kim SJ, et al. Anti-breast cancer activity of Fine Black ginseng (Panax ginseng Meyer) and ginsenoside Rg5. J Ginseng Res. 2015 Apr;39(2):125-34.
Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 inhibits VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS). Ginsenoside Rg2 also reduces Aβ1-42 accumulation.
IC50 Target[1][2]
NF-κB
;
Aβ1-42
;
体外研究 (In Vitro)
Ginsenoside Rg2 prevents the decrease of IκB expression stimulated with lipopolysaccharide (LPS). IκB dissociation from RelA-p50 complex is crucial for NF-κB activity. Ginsenoside Rg2, protopanaxatriol, inhibits vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression stimulated with LPS from human umbilical vein endothelial cell (HUVEC). The inhibition of VCAM-1 and ICAM-1 expression by Ginsenoside Rg2 is in a concentration-dependent manner, significantly. Treatment of endothelial cells with LPS (1µg/mL) decreases IκBα expression. By 1 hr after LPS treatment, significant decrease of IκBα is attained. To determine whether LPS-stimulated IκBα expression is affected by Ginsenoside Rg2, endothelial cells are treated for 1 hr with Ginsenoside Rg2 (1~50 µM) prior to LPS (1 µg/mL) stimulation for 1 hr. Ginsenoside Rg2 reverses the decrease of LPS-induced IκBα expression in a concentration-dependent manner, significantly. The adhesion of THP-1 cells to endothelial cells is measured using quantitative monolayer adhesion assay. The adhesion of THP-1 cells onto endothelial cells are increased to five folds by LPS (1 µg/mL) stimulation for 8 hrs. Ginsenoside Rg2 (1~50 µM) inhibits the adhesion of THP-1 cells to endothelial cells stimulated with LPS, in a concentration-dependent manner[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
G-Rg1 and Ginsenoside Rg2 (G-Rg2) reduce the escape latencies on the last two training days compared to the Alzheimer’s disease (AD) model group (p<0.05). In the spatial exploration test, the total time spent in the target quadrant and the number of mice that exactly crossed the previous position of the platform are clearly shorter and lower, respectively, in the AD model group mice than in the normal control group mice (p<0.01), a trend that is reversed by treatment with G-Rg1 and Ginsenoside Rg2 (G-Rg1, p<0.01; Ginsenoside Rg2, p<0.05). Treatment with G-Rg1 and Ginsenoside Rg2 effectively improve cognitive function of the mice that have declined due to AD. G-Rg1 and Ginsenoside Rg2 reduce Aβ1-42 accumulation in APP/PS1 mice. In the G-Rg1 and Ginsenoside Rg2 treated mice, the pathological abnormalities observed in the APP/PS1 mice are gradually ameliorated. Clear nucleoli and light brown, sparsely scattered Aβ deposits are visible[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
785.01
Formula
C42H72O13
CAS 号
52286-74-5
中文名称
人参皂苷 Rg2;人参皂苷 Rg2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Powder
-20deg;C
3 years
4deg;C
2 years
In solvent
-80deg;C
6 months
-20deg;C
1 month
溶解性数据
In Vitro:;
DMSO : 100 mg/mL (127.39 mM; ultrasonic and warming and heat to 60°C)
[1]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013 Apr;17(2):133-7.
[2]. Li N, et al. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer’s disease. J Ginseng Res. 2016 Jan;40(1):9-17.
[3]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013;17(2):133-137.
Cell Assay
HUVECs ares grown in EBM-2 containing 10% FBS at a density of 2.0×105 cells/well on 24-well plates. Endothelial cells at 90~95% confluence are treated with Ginsenoside Rg2 (1, 20, 50 µM) for 1 hr prior to 1 µg/mL of LPS stimulation for 8 hr. THP-1 cells are labeled with Calcein-AM (5 µM) in RPMI 1640 medium containing 10% FBS for 30 min. After extensive washing with PBS, the labeled THP-1 cells are seeded at a density of 5.0×105 cells/well onto endothelial cells which are treated with the Rg2 and/or LPS and, then, incubated for 1 hr at 37°C while gentle shaking. After incubation, non-adherent cells are removed by gentle washing two times with PBS. Photograph images are obtained at 485 nm excitation and 538 nm emission using a SPOT II digital camera-attached fluorescence microscope[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Male APP/PS1 mice, weighing 20±2 g, and male C57BL/6J mice, weighing 20±2 g, are used. The animals are maintained in an air-conditioned animal center at 23±2°C and a relative humidity of 50±10%, with a natural light-dark cycle. Food and water are available ad libitum. After acclimatization for 1 wk, the mice are divided into four groups (n=10 in each group): the normal control group, the AD model group, the G-Rg1 group, and the Ginsenoside Rg2 group. According to the concentration-response curves, the mice in the G-Rg1 and Ginsenoside Rg2 groups are injected intraperitoneally once daily with G-Rg1 and Ginsenoside Rg2 (30 mg/kg), respectively, dissolved in saline. The mice in the AD model group (APP/PS1 mice) and the normal control group (C57BL/6J nontransgenic littermates) are treated with isodose saline (0.9% w/v). All mice are treated for 1 mo before brain metabolite profiling.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013 Apr;17(2):133-7.
[2]. Li N, et al. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer’s disease. J Ginseng Res. 2016 Jan;40(1):9-17.
[3]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013;17(2):133-137.