Ginsenoside C-Y, a natural antioxidant, possesses antiphotoaging and antimelanogenesis activities[1].
分子量
754.99
Formula
C41H70O12
CAS 号
83480-65-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Xiao-Yi Liu, et al. Antiphotoaging and Antimelanogenesis Properties of Ginsenoside C-Y, a Ginsenoside Rb2 Metabolite from American Ginseng PDD-ginsenoside. Photochem Photobiol. 2019 Nov;95(6):1412-1423.
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 Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
IC50 Target[1]
Caspase-8
;
Caspase-9
;
Apoptosis
;
Human Endogenous Metabolite
;
体外研究 (In Vitro)
Ginsenoside Rh2 induces the activation of two initiator caspases, caspase-8 and caspase-9 in human cancer cells. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner and is therefore a promising candidate for anti-tumor drug development. Ginsenoside Rh2 triggers p53-dependent Fas expression and consequent activation of caspase-8 and p53-independent caspase-9-mediated intrinsic pathway to cause cancer cell death.The cytotoxic activity of Ginsenoside Rh2 in the human tumor cell lines HeLa, SK-HEP-1, SW480, and PC-3 is assessed by MTT. The cell viability of HeLa cells is remarkably inhibited by Ginsenoside Rh2, with an IC50 value of 2.52 μg/mL, whereas SK-HEP-1 and SW480 cells are less sensitive to Ginsenoside Rh2, with IC50 values of 3.15 μg/mL and 4.06 μg/mL, respectively. PC-3 cells are the least vulnerable to Ginsenoside Rh2, with an IC50 value of 7.85 μg/mL, 3-fold higher than HeLa cells[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
A total of 15 days following B16-F10 cell injection, tumor sizes from the 3 tumor bearing groups are measured. The tumor sizes in the G-L group and G-H group (G-L and G-H refer to a low or high dose of ginsenoside Rh2 injection) are reduced compared with the tumor group (P<0.05). The survival analysis reveals that the Ginsenoside Rh2 treated groups survive longer than the untreated tumor group and the effect is dose-dependent (P<0.05)[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
622.87
Formula
C36H62O8
CAS 号
78214-33-2
中文名称
人参皂苷 Rh2；人参皂苷 Rh2
运输条件
Room temperature in continental US; may vary elsewhere.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
*以上所有助溶剂都可在 MCE 网站选购。
参考文献
[1]. Guo XX, et al. p53-dependent Fas expression is critical for Ginsenoside Rh2 triggered caspase-8 activation in HeLa cells. Protein Cell. 2014 Mar;5(3):224-34.
[2]. Wang M, et al. Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model. Oncol Lett. 2017 Feb;13(2):681-685.
Kinase Assay [1]
HeLa, SK-HEP-1, SW480, and PC-3 cells are treated with Ginsenoside Rh2 (7.5 μg/mL) in serum free media for indicated time periods and then are harvested. Fifty micrograms of cell lysates are incubated with 200 nM Ac-DEVD-AFC (for caspase-3), Ac-IETD-AFC (for caspase-8), and Ac-LEHD-AFC (for caspase-9) in a reaction buffer containing 20 mM HEPES, pH 7.4, 100 mM NaCl, 10 mM DTT, 0.1% CHAPS, and 10% sucrose at 37°C for 1 h. The reaction is monitored by fluorescence emission at 535 nm and excitation at 405 nm[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
Determination of cell viability is performed by using MTT assay, which is used to calculate the growth inhibition induced by increasing concentrations of drug. Briefly, exponentially growing HeLa, SK-HEP-1, SW480, and PC-3 cells are seeded into a 96-well plate at 1×104 cells/well in triplicate. After incubation for 24 h, cells are treated with increasing concentration of Ginsenoside Rh2 (1, 2.5, 5, 7.5 and 10 μg/mL) in serum free media for 48 h. At the end of treatment, 20 μL of MTT (5 mg/mL) is added to each well and incubated for an additional 4 h. The formazan grains formed by viable cells are solubilized with DMSO, and the color intensity is measured at 550 nm with an ELISA reader[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Male C57BL6 mice (3-4 weeks old) are randomly arranged into 4 groups of 80 mice: Tumor group, G-L group, G-H group and Control group. G-L and G-H refer to a low or high dose of ginsenoside Rh2 injection. For the tumor group, G-L group and G-H group, the B16-F10 cell line is injected into the mice. These 3 groups become tumor bearing groups. For the control group, the same volume of PBS is injected instead. Ginsenoside Rh2 is injected into the left back of mice in the G-L and G-H groups. The dose for the G-H group is 0.5 mg/kg or 0.2 mg/kg for G-L group, every 2 days after day 5. PBS is injected in the tumor and control groups at the same time points.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Guo XX, et al. p53-dependent Fas expression is critical for Ginsenoside Rh2 triggered caspase-8 activation in HeLa cells. Protein Cell. 2014 Mar;5(3):224-34.
[2]. Wang M, et al. Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model. Oncol Lett. 2017 Feb;13(2):681-685.
Ginsenoside Rb1, a main constituent of the root of Panax ginseng, inhibits Na+, K+-ATPase activity with an IC50 of 6.3±1.0 μM. Ginsenoside also inhibits IRAK-1 activation and phosphorylation of NF-κB p65 .
IC50 Target[1][2][3][6]
Na+, K+-ATPase
6.3 mu;M (IC50)
IRAK-1
;
p65
;
Autophagy
;
Mitophagy
;
HSV-1
;
体外研究 (In Vitro)
Rat brain microsomal Na+, K+-ATPase activity is inhibited significantly and rapidly by Ginsenoside Rb1. The IC50 of Ginsenoside Rb1 for Na+,K+-ATPase is 6.3±1.0 μM. The inhibition is enhanced with increasing the concentration of Ginsenoside Rb1 or decreasing that of Na+ and K+. Kinetic analysis reveals that Ginsenoside is an uncompetitive inhibitor with respect to ATP[1]. Ginsenoside Rb1 significantly inhibits the activation of interleukin-1 receptor-associated kinase-1 (IRAK-1), IKK-β, NF-κB, and MAP kinases (ERK, JNK, and p-38); however, interaction between LPS and Toll-like receptor-4, IRAK-4 activation and IRAK-2 activation are unaffected[2]. Ginsenoside Rb1 is an ingredient of a Chinese medicine Panax ginseng. Ginsenoside Rb1 is a major bioactive compound in the regulating pregnane X receptor (PXR)/NF-κB signaling. Ginsenoside Rb1 is the compound with potent anti-inflammatory activity in ginseng saponin extract (GSE). The concentration for Ginsenoside Rb1 (10 μM) is optimized from a preliminary study to ensure sufficient anti-inflammatory activity and without apparent cytotoxicity. Ginsenoside Rb1 significantly reduces TNF-α-induced upregulation of IL-1β and iNOS mRNA levels, and restores the mRNA levels of PXR and CYP3A4 in LS174T cells. TNF-α causes a significant reduction in PXR protein levels and increase in the ratio of phosphorylated to total NF-κB p65, both of which are significantly abrogated by Ginsenoside Rb1[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Rb1 at the both doses of 30 mg/kg and 60 mg/kg significantly attenuates the histological lung injury. Ginsenoside Rb1 at the dose of 30 mg/kg and 60 mg/kg both significantly attenuates the histological intestine injury[4]. Ginsenoside Rb1 (Rb1), an ingredient of a Chinese medicine Panax ginseng, has beneficial effects on mesentery microvascular hyperpermeability induced by Lipopolysaccharide (LPS) and the underlying mechanisms. In some rats, Ginsenoside Rb1 (5 mg/kg per hour) is administrated through the left jugular vein 30 min after LPS infusion. Ginsenoside Rb1 decreases caveolae number in endothelial cells of microvessels. Ginsenoside Rb1 ameliorates microvascular hyperpermeability after the onset of endotoxemia and improves intestinal edema through inhibiting caveolae formation and junction disruption, which is correlated to suppression of NF-κB and Src activation[5].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1109.29
Formula
C54H92O23
CAS 号
41753-43-9
中文名称
人参皂苷 Rb1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Cao J, et al. Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na+,K+-ATPase activity. Zhongguo Yao Li Xue Bao. 1990 Jan;11(1):10-4.
[2]. Zhang J, et al. Ginsenosides Regulate PXR/NF-κB Signaling and Attenuate Dextran Sulfate Sodium-Induced Colitis. Drug Metab Dispos. 2015 Aug;43(8):1181-9.
[3]. Joh EH, et al. Ginsenoside Rb1 and its metabolite compound K inhibit IRAK-1 activation–the key step of inflammation. Biochem Pharmacol. 2011 Aug 1;82(3):278-86.
[4]. Jiang Y, et al. Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice. Oxid Med Cell Longev. 2015;2015:843721.
[5]. Zhang Y, et al. Ginsenoside Rb1 ameliorates lipopolysaccharide-induced albumin leakage from rat mesenteric venules by intervening in both trans- and paracellular pathway. Am J Physiol Gastrointest Liver Physiol. 2014 Feb 15;306(4):G289-300.
Cell Assay [3]
LS174T cells are seeded in cell imaging dish. After overnight incubation, cells are treated with GSE (100 μg/mL), Ginsenoside Rb1 (10 μM), or CK (10 μM) for 3 hours, followed by an additional incubation with or without TNF-α (20 ng/ml) for 6 hours. At the end of the incubation, cells are harvested and fixed with 4% paraformaldehyde solution at 20°C for 20 minutes. After washing in PBS, cells are permeabilized with 0.2% Triton X-100 in PBS at room temperature for 5 minutes. After incubation in blocking buffer containing 0.1% Triton X-100 and 5% bovine serum albumin, cells are incubated with rabbit NF-κB p65 antibody at 4°C overnight and then with Alexa Fluor 488-conjugated anti-rabbit IgG antibody at room temperature for 30 minutes in 1% bovine serum albumin in PBS. Fluorescence photographs are obtained using a Zeiss 710 confocal microscope[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [4][5]
Mice[4] Male C57BL/6 mice (9-12 weeks old; 17-22 g) are randomly allocated into eight groups (n=8 in each group): (1) Sham surgical preparation including isolation of the superior mesenteric artery (SMA) without occlusion is performed (Sham); (2) mice are subjected to II/R without treatment (II/R); (3) mice are subjected to II/R with treatment of normal saline 10 minutes before reperfusion (II/R+NS); (4), (5) mice are treated with 30 mg/kg (II/R+Rb1-30) or 60 mg/kg (II/R+Rb1-60) Ginsenoside Rb1, in which surgery is performed as in the II/R group with administration of the Ginsenoside Rb1 intraperitoneally 10 minutes before reperfusion; (6) mice are subjected to Sham surgery and treated with ATRA (ATRA+Sham), which is the inhibitor of Nrf2/ARE signaling pathway; (7) mice are subjected to II/R and treated with ATRA (ATRA+II/R); (8) mice are subjected to II/R and treated with ATRA and 60 mg/kg Ginsenoside Rb1 as group 5 (ATRA+II/R+Rb1-60). During the last two weeks before the operation, the mice in the group 6, 7, 8 receive ATRA i.p. daily at 10 mg/kg and fed on a vitamin A-deficient diet, and the mice in the other groups receive the equivalent volume of corn oil and fed on a control normal diet. Rats[5] Male Wistar rats weighing 200-250 g are used. The rats are randomly divided into four groups, 26 animals in each. After being anesthetized with urethane (2 g/kg body wt im), the left femoral vein and left jugular vein of the rat are cannulated. In the LPS group, LPS solution in saline is infused (5 mg/kg per hour) for 90 min via the left femoral vein. The vehicle, instead of LPS solution, is administrated in Sham and Ginsenoside Rb1 alone (Rb1, 5 mg/kg) groups. In the Rb1 posttreatment (LPS+Rb1) group, Ginsenoside Rb1 solution is infused continuously through the left jugular vein 30 min after LPS administration at the dose of 5 mg/kg. Ginsenoside Rb1 solution and the same volume of saline are infused in Ginsenoside Rb1 and Sham groups, respectively, without subsequent LPS administration. In a separate set of experiments, the rats are anesthetized with 2% penobarbital sodium (60 mg/kg body wt ip), and saline, LPS, and Ginsenoside Rb1. After recovery from anesthesia, the animals are allowed access to water and rodent chow, and survival rate is recorded over time until 4 days after LPS stimulation.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Cao J, et al. Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na+,K+-ATPase activity. Zhongguo Yao Li Xue Bao. 1990 Jan;11(1):10-4.
[2]. Zhang J, et al. Ginsenosides Regulate PXR/NF-κB Signaling and Attenuate Dextran Sulfate Sodium-Induced Colitis. Drug Metab Dispos. 2015 Aug;43(8):1181-9.
[3]. Joh EH, et al. Ginsenoside Rb1 and its metabolite compound K inhibit IRAK-1 activation–the key step of inflammation. Biochem Pharmacol. 2011 Aug 1;82(3):278-86.
[4]. Jiang Y, et al. Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice. Oxid Med Cell Longev. 2015;2015:843721.
[5]. Zhang Y, et al. Ginsenoside Rb1 ameliorates lipopolysaccharide-induced albumin leakage from rat mesenteric venules by intervening in both trans- and paracellular pathway. Am J Physiol Gastrointest Liver Physiol. 2014 Feb 15;306(4):G289-300.
Ginsenoside Ro (Polysciasaponin P3; Chikusetsusaponin 5; Chikusetsusaponin V) exhibits a Ca2+-antagonistic antiplatelet effect with an IC50 of 155 μM. Ginsenoside Ro reduces the production of TXA2 more than it reduces the activities of COX-1 and TXAS.
IC50 & Target[1][2]
TXA2
Ca2+
体外研究 (In Vitro)
Ginsenoside Ro in Panax ginseng is a beneficial novel Ca2+-antagonistic compound and may prevent platelet aggregation-mediated thrombotic disease. Ginsenoside Ro dose-dependently reduces thrombin-stimulated platelet aggregation, and IC50 is approximately 155 μM[1]. Ginsenoside Ro inhibits TXA2 production to abolish thrombin-induced platelet aggregation. Thromboxane A2 (TXA2) induces platelet aggregation and promotes thrombus formation. Ginsenoside Ro dose-dependently (50-300 μM) reduces the TXB2 level that is induced by thrombin; Ginsenoside Ro (300 μM) inhibits the thrombin-mediated elevation in TXB2 level by 94.9%. COX-1 activity in the absence of Ginsenoside Ro (negative control) is 2.3±0.1 nmol/mg protein. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, COX-1 activity is reduced by 26.4% of that of the negative control. TXA2 synthase (TXAS) activity in the absence of Ginsenoside Ro (negative control) is 220.8±1.8 ng/mg protein/min. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, TXAS activity is reduced by 22.9% of that of the negative control. The inhibitory effect of Ginsenoside Ro (300 μM) on TXB2 production (94.9%) is significantly higher than those on COX-1 (26.4%) and TXAS (22.9%) activities[2]. To assess the toxicity of Ginsenoside Ro in Raw 264.7 cells, they are first treated with various concentrations (10 μM, 50 μM, 100 μM, and 200 μM) of Ginsenoside Ro for 24 h. Ginsenoside Ro exhibits no significant dose dependent toxicity. The effect of Ginsenoside Ro is next determined on cell viability and ROS levels, a marker of oxidative stress, following treatment with 1 μg/mL LPS. LPS reduces cell viability by ∼70% compared with nontreated controls. Pretreatment with 100 μM and 200 μM Ginsenoside Ro for 1 h prior to 1 μg/mL LPS incubation for 24 h leads to a significant increase in cell viability. The changes in ROS levels and NO production are consistent with the effects of Ginsenoside Ro on viability[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Ro dissolved in water is administrated by gavage to mice at doses of 25 and 250 mg/kg/day for 4 days before i.v. injection of HT29 in order to keep blood concentrations of Ginsenoside Ro above a certain level before HT29 i.v. injection followed by 40 days of oral administration of Ginsenoside Ro to the mice. After 38 days of treatment, the animals are euthanized, and the number of pulmonary metastatic nodules is counted in addition to evaluation of toxicity of Ginsenoside Ro and mouse pathology by HT29. Ginsenoside Ro (250 mg/kg/day) produces a significant decrease in the number of tumor nodules on the lung surface, yielding inhibition rates of 88% (P < 0.01)[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
957.11
Formula
C48H76O19
CAS 号
34367-04-9
中文名称
人参皂苷 Ro；人参皂苷 Ro
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Kwon HW, et al. Inhibitory Effects of Cytosolic Ca2+ Concentration by Ginsenoside Ro Are Dependent on Phosphorylation of IP3RI and Dephosphorylation of ERK in Human Platelets. Evid Based Complement Alternat Med. 2015;2015:764906.
[2]. Jung-HaeShin, et al. Inhibitory effects of thromboxane A2 generation by ginsenoside Ro due to attenuation of cytosolic phospholipase A2 phosphorylation and arachidonic acid release. J Ginseng Res. 9 Jan 2018.
[3]. Kim S, et al. Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells. J Ginseng Res. 2015 Oct;39(4):365-70.
[4]. Jiang Z, et al. The traditional Chinese medicine Achyranthes bidentata and our de novo conception of its metastatic chemoprevention: from phytochemistry to pharmacology. Sci Rep. 2017 Jun 20;7(1):3888.
Kinase Assay [2]
The microsomal fraction of platelets is preincubated with Ozagrel (11 nM, IC50), a positive control, or with various concentrations of Ginsenoside Ro and other reagents at 37°C for 5 min. The reaction is initiated by adding prostaglandin H2, and the samples are incubated at 37°C for 1 min; the reaction is terminated by adding citric acid (1 M). After neutralization with 1 N NaOH, the amount of TXB2 is determined using a TXB2 EIA kit[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [3]
Cell viability is determined with an MTT assay kit. Briefly, Raw 264.7 cells are plated in 48-well plates at a density of 2.0×104 cells per well, incubated for 24 h, and treated with various concentrations of Ginsenoside Ro for 24 h. How 1 h of pretreatment with Ginsenoside Ro (50 μM, 100 μM, and 200 μM) affects the viability of Raw 264.7 cells is then investigated treated with 1 μg/mL LPS for 24 h. After the incubation period, 10 μL of MTT reagent is added to each well and incubated for 3 h at 37°C in 5% CO2. The resulting formazan crystals are subsequently dissolved in MTT solubilization solution. The absorbance is determined at 540 nm using a microplate reader[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [4]
Mice[4] Female BALB/c mice (20-25 g, 6-8 weeks old) are used. The experimental model of lung metastasis is established by tail vein injection of HT29 cells to mimic the dissemination of CTCs. HT29 cells in the number of 2×106 cells in 0.2 mL PBS are infected into the tail vein of six-week-old female Balb/c mice. Before the HT29 inoculation, oral gavage pretreatment of PBS-suspended B (Ginsenoside Ro) is given daily for 4 days, followed by a 40-day treatment. Treatment groups (N = 10) include: 0 mg/kg, 25 mg/kg and 250 mg/kg Ginsenoside Ro. Body weight is measured and recorded every four days. Mice are sacrificed after 40 days of tumor metastasis and growth and 44 days of treatment with B. The number of surface lung metastasis nodules is evaluated in each treatment group. Slides with 4-5 μm thick lung section are prepared, paraffin embedded and then stained with hematoxylin and eosin[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Kwon HW, et al. Inhibitory Effects of Cytosolic Ca2+ Concentration by Ginsenoside Ro Are Dependent on Phosphorylation of IP3RI and Dephosphorylation of ERK in Human Platelets. Evid Based Complement Alternat Med. 2015;2015:764906.
[2]. Jung-HaeShin, et al. Inhibitory effects of thromboxane A2 generation by ginsenoside Ro due to attenuation of cytosolic phospholipase A2 phosphorylation and arachidonic acid release. J Ginseng Res. 9 Jan 2018.
[3]. Kim S, et al. Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells. J Ginseng Res. 2015 Oct;39(4):365-70.
[4]. Jiang Z, et al. The traditional Chinese medicine Achyranthes bidentata and our de novo conception of its metastatic chemoprevention: from phytochemistry to pharmacology. Sci Rep. 2017 Jun 20;7(1):3888.
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.
Ginsenoside F1 是 Ginsenoside Rg1 的酶促修饰衍生物，Ginsenoside F1 竞争性抑制 CYP3A4，对 CYP2D6 具有较弱的抑制作用。
Ginsenoside F1 Chemical Structure
CAS No. : 53963-43-2
规格
价格
是否有货
数量
10 mM * 1 mL in DMSO
￥984
In-stock
5 mg
￥700
In-stock
10 mg
￥1200
In-stock
50 mg
￥3600
In-stock
100 mg
询价
200 mg
询价
* Please select Quantity before adding items.
Ginsenoside F1 相关产品
•相关化合物库:
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生物活性
Ginsenoside F1, an enzymatically modified derivative of Ginsenoside Rg1, demonstrates competitive inhibition of CYP3A4 activity and weaker inhibition of CYP2D6 activity.
IC50 & Target
CYP3A4
Human Endogenous Metabolite
体外研究 (In Vitro)
Ginsenoside F1 has been shown to flaunt anticancer, anti-aging, and antioxidant effects and has demonstrated competitive inhibition of CYP3A4 activity and weaker inhibition of CYP2D6 activity. The cell viabilities are 68% at the highest concentration of ginsenoside F1 (200 μM) in MTT assays[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
ApoE-/- mice are fed a high fat diet and orally treated with Ginsenoside F1 (50 mg/kg/day) for 8 weeks. Ginsenoside F1 treated mice significantly reduce the lesion size compared with model group mice[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
638.87
Formula
C36H62O9
CAS 号
53963-43-2
中文名称
人参皂苷 F1；人参皂苷 F1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Wang DD, et al. Rare ginsenoside Ia synthesized from F1 by cloning and overexpression of the UDP-glycosyltransferase gene from Bacillus subtilis: synthesis, characterization, and in vitromelanogenesis inhibition activity in BL6B16 cells. J Ginseng Res. 2018 Jan;42(1):42-49.
[2]. Qin M, et al. Ginsenoside F1 Ameliorates Endothelial Cell Inflammatory Injury and Prevents Atherosclerosis in Mice through A20-Mediated Suppression of NF-kB Signaling. Front Pharmacol. 2017 Dec 22;8:953.
Kinase Assay [1]
Glycosylation ability is assayed with overexpressed BSGT1 enzyme and F1. The reaction mixtures contain 100 μL of 0.5 mM F1 and 100 μL of 2.5 mM UDP-glucose and 800 μL of purified enzyme (final concentration at 0.1 mg/mL) (pH 7.0). The mixtures are incubated at 30°C for 24 h. Moreover, three groups of controls are incubated under the same conditions: (1) control 1 (C1) consists of Ginsenoside F1 with BSGT1; (2) control 2 (C2) consists of BSGT1 with UDP-glucose; and (3) control 3 (C3) consists of Ginsenoside F1 with UDP-glucose[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
B16BL6 cells are cultured in Dulbecco’s modified Eagles medium supplemented with 10% fetal bovine serum and 1% Penicillin-Streptomycin at 37°C in a humidified 95% air/5% CO2 atmosphere. Cell viability is determined for Ginsenoside F1 and metabolite 1 using MTT conversion to formazan. Cells are seeded at a density of 1×105 cells/well in a 96-well plate, cultured for 24 h, and treated with various concentrations from 1 μM to 200 μM of Ginsenoside F1 and metabolite 1 for 5 d. Finally, 10 μL of MTT (5 mg/mL in PBS) is added to each well. Cells are incubated at 37°C for 3 h, and then DMSO (100 μL) is added to dissolve the formazan crystals. The absorbance is measured at 570 nm with the reference wavelength of 630 nm using an ELISA reader[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Six-week-old (17±1 g) male C57BL/6 mice and ApoE-/- mice with a C57BL/6 background are maintained in a temperature-controlled facility (temperature: 22±1°C; humidity: 60%) with a 14 h light/10 h dark cycle in conventional cages. Forty mice are randomly divided into four experimental groups (n=10/group): (I) C57BL/6 N mice, the control group; (II) ApoE-/- mice group; (III) ApoE-/- mice+ Ginsenoside F1 group; (IV) ApoE-/- mice+Probucol group. All mice are fed with a high fat diet (HFD, 0.3% cholesterol and 20% pork fat) for 8 weeks. Ginsenoside F1 (50 mg/kg/day, i.g.) and Probucol (2 g/kg, i.g.) are dissolved in carboxymethyl cellulose sodium (CMC-Na). Oral administration is given to mice every day for 8 weeks. The control and model groups receive the aseptic 0.5% CMC-Na treatment every day (i.g., 0.1 mL/10g) [2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Wang DD, et al. Rare ginsenoside Ia synthesized from F1 by cloning and overexpression of the UDP-glycosyltransferase gene from Bacillus subtilis: synthesis, characterization, and in vitromelanogenesis inhibition activity in BL6B16 cells. J Ginseng Res. 2018 Jan;42(1):42-49.
[2]. Qin M, et al. Ginsenoside F1 Ameliorates Endothelial Cell Inflammatory Injury and Prevents Atherosclerosis in Mice through A20-Mediated Suppression of NF-kB Signaling. Front Pharmacol. 2017 Dec 22;8:953.
Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures[1]. Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB[2]. Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis[1]. Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway[3].
体外研究 (In Vitro)
Ginsenoside Rk1 (0-40 μM; 6 hours) inhibits MCP-1 and TNF-α mRNA induced by lipopolysaccharide (LPS), expression of IL-1β is inhibited at 40 μM[2]. Ginsenoside Rk1 (0-40 μM; 24 hours) inhibits phosphorylation of JAK2 and STAT3 (Tyr705 and Ser727) in LPS-induced RAW264.7 cells in a dose-dependent manner[2]. Ginsenoside Rk1 (0-160 μM; 48 hours) results in cell viability significant decrease 75.52 ± 2.51% (40 μM), 52.72 ± 2.54% (80 μM), 17.41 ± 2.94% (120 μM)and 12.63 ± 3.24% (160 μM) compared with control[3]. Ginsenoside Rk1 (0-120 μM; 24 hours) increases G0/G1 phase proportion accompanied with S and G2/M phase proportion decrease in MDA-MB-231 cells[3]. Ginsenoside Rk1 (0-120 μM; 24 hours) promotes the percentage of apoptotic cells in a dose-dependent manner, exhibits to reduction of cell number with nucleus fragmentation, condensation and apoptotic body formation[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
RT-PCR[2]
Cell Line:
RAW264.7 cells
Concentration:
10 μM, 20 μM, 40 μM
Incubation Time:
6 hours
Result:
Inhibited JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells.
Western Blot Analysis[2]
Cell Line:
RAW264.7 cells
Concentration:
10 μM, 20 μM, 40 μM
Incubation Time:
6 hours
Result:
Inhibited JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells
Cell Viability Assay[3]
Cell Line:
MDA-MB-231 cells
Concentration:
0 μM, 40 μM, 80 μM, 120 μM
Incubation Time:
48 hours
Result:
Inhibited MDA-MB-231 cells proliferation in a dose- and time-dependent manner.
Cell Cycle Analysis[3]
Cell Line:
MDA-MB-231 cells
Concentration:
0 μM, 40 μM, 80 μM, 120 μM
Incubation Time:
24 hours
Result:
Induced G0/G1 phase arrest.
Apoptosis Analysis[3]
Cell Line:
MDA-MB-231 cells
Concentration:
0 μM, 40 μM, 80 μM, 120 μM
Incubation Time:
24 hours
Result:
Induced apoptosis in MDA-MB-231 cells.
分子量
767.00
Formula
C42H70O12
CAS 号
494753-69-4
中文名称
人参皂苷
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Elshafay A, et al. Ginsenoside Rk1 bioactivity: a systematic review. PeerJ. 2017 Nov 17;5:e3993.
[2]. Yu Q,et al. Ginsenoside Rk1 suppresses pro-inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells by inhibiting the Jak2/Stat3 pathway. Chin J Nat Med. 2017 Oct;15(10):751-757.
[3]. Hong Y, et al. Ginsenoside Rk1 induces cell cycle arrest and apoptosis in MDA-MB-231 triple negative breast cancer cells. Toxicology. 2019 Apr 15;418:22-31.
