Ginsenoside Rg4 是一种从 Panax ginseng C. A. Meyer 的叶子中分离出来的一种主要的人参三醇型人参皂苷。人参三醇型人参皂苷 (如 Ginsenoside Rg4) 具有多种生物活性，包括防腐，抗糖尿病，伤口愈合，免疫刺激和抗氧化活性。
Ginsenoside Rg4 Chemical Structure
CAS No. : 126223-28-7
规格
价格
是否有货
1 mg
￥1350
询问价格 货期
5 mg
￥3400
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生物活性
Ginsenoside Rg4 is a major protopanaxatriol type ginsenoside isolated from the leaves of Panax ginseng C. A. Meyer. The protopanaxatriol type ginsenosides (such as Ginsenoside Rg4) exhibits various biological activities including anti-septic, anti-diabetic, wound healing, immune-stimulatory, and anti-antioxidant activity[1][2].
分子量
767.00
Formula
C42H70O12
CAS 号
126223-28-7
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]. S L Zhang, et al. A New Minor Saponin From the Leaves of Panax Ginseng C. A. Meyer. Yao Xue Xue Bao. 1989;24(11):877-9.
[2]. Wonhwa Lee, et al. Inhibitory Effects of Protopanaxatriol Type Ginsenoside Fraction (Rgx365) on Particulate Matter-Induced Pulmonary Injury. J Toxicol Environ Health A. 2019;82(5):338-350.
Panaxadiol is found in the roots of Panax ginseng, activities neuroprotective and anti-tumour functions. Panaxadiol inhibits programmed cell death-ligand 1(PD-L1) expression and tumour proliferation[1].
分子量
460.73
Formula
C30H52O3
CAS 号
19666-76-3
中文名称
人参二醇；人参萜二醇
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Wang Z, et al. Panaxadiol inhibits programmed cell death-ligand 1 expression and tumour proliferation via hypoxia-inducible factor (HIF)-1α and STAT3 in human colon cancer cells. Pharmacol Res. 2020;155:104727.
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.
Ginsenoside Rb2 is one of the main bioactive components of ginseng extracts. Rb2 can upregulate GPR120 gene expression. Ginsenoside Rb2 has antiviral effects.
IC50 Target
Human Endogenous Metabolite
;
体外研究 (In Vitro)
Ginsenoside Rb2 pre-treatment enhances the anti-inflammatory effect of α-linolenic acid (ALA) and that the enhancing effect is strictly dependent on GPR120 activation. Ginsenoside Rb2 exerts anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated mouse macrophage RAW264.7 cells in vitro by increasing GPR120 expression and subsequently enhancing ω-3 fatty acid-induced GPR120 activation. Ginsenoside Rb2 improves glucose metabolism in hepatocytes by activating AMPK and reduces cholesterol and triacylglycerol levels in 3T3-L1 cells by reducing oxidative damage. Ginsenoside Rb2 exerts anti-apoptosis effects in murine bone marrow-derived mesenchymal stem cells (BMMSCs). MTT assay results show no obvious cytotoxicity of Ginsenoside Rb2 (up to 100 μM) toward RAW264.7 cells in the absence or presence of ALA. The influence of Rb2 on GPR120 expression in RAW264.7 macrophages is investigated by treating the cells with Ginsenoside Rb2 (0.1-100 μM) for 12 h followed by harvesting and lysis. Subsequent Western blot analysis shows that expression of GPR120 is dose-dependently upregulated by Ginsenoside Rb2. Real-time PCR results indicate that incubation of RAW264.7 macrophages with Ginsenoside Rb2 (10 μM) for 12 h leads to a 2.8-fold increase in GPR120 mRNA expression. In addition, this increase in GPR120 expression stimulated by Ginsenoside Rb2 is time dependent and begins as early as 6 h. These results indicate that Rb2 upregulates GPR120 expression in a dose- and time-dependent manner in RAW264.7 macrophages[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Ginsenoside Rb2 is an antiviral reagent to protect against rotavirus (RV) infection. When various dosages of Ginsenoside Rb2 (25 to 250 mg/kg) are administered 3, 2 or 1 days before virus challenge, treatment with this Ginsenoside at the dosage of 75 mg/kg 3 days before virus infection most effectively reduces rotavirus (RV) -induced diarrhea. In addition, consecutive administration of Ginsenoside Rb2 (75 mg/kg) 3, 2, and 1 day before virus infection is more effective than single administration on day-3. The consecutive administration of Ginsenoside Rb2 also reduces virus titers in the bowels of RV-infected mice[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1079.27
Formula
C53H90O22
CAS 号
11021-13-9
中文名称
人参皂苷 Rb2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Huang Q, et al. Ginsenoside Rb2 enhances the anti-inflammatory effect of ω-3 fatty acid in LPS-stimulated RAW264.7 macrophages by upregulating GPR120 expression. Acta Pharmacol Sin. 2017 Feb;38(2):192-200.
[2]. Yang H, et al. Ginsenoside-Rb2and 20(S)-Ginsenoside-Rg3 from Koreanred ginseng prevent rotavirus infection in newborn mice. J Microbiol Biotechnol. 2018 Jan 11.
Cell Assay [1]
Cell viability is determined using the MTT assay. RAW264.7 cells (2×104 cells/well) are plated in 96-well plates and cultured overnight in growth medium. The cells are then incubated with Ginsenoside Rb2 (0.1, 1, 10 and 100 μM) at the indicated concentrations in the absence or presence of ALA for 48 h before addition of the MTT reagent (0.5 mg/mL). After incubation for 4 h, the medium is removed, and the formazan crystals formed are dissolved with 100 μL DMSO. Absorbance at a wavelength of 492 nm is measured using a FlexStation 3[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Groups of five BALB/c newborn mice are inoculated p.o. with RV-SA11 (1.5×106 plaque-forming units (PFU)/mouse) and administered p.o. with the indicated doses of Ginsenoside Rb2 on the indicated days. In order to examine the protective effect of Ginsenoside Rb2 on RV infection, newborn mice are treated orally with 75 mg/kg of this Ginsenoside 3, 2 or 1 day before RV infection, and the severity of diarrhea of RV-infected mice i calculated. In addition, in an experiment in which various doses of Ginsenoside Rb2 ranging from 25 to 250 mg/kg are administered to mice 3 days before RV infection, Ginsenoside Rb2 at the dose of 75 mg/kg elicits higher protective activity compared to either of the dose of 25 to 250 mg/kg.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Huang Q, et al. Ginsenoside Rb2 enhances the anti-inflammatory effect of ω-3 fatty acid in LPS-stimulated RAW264.7 macrophages by upregulating GPR120 expression. Acta Pharmacol Sin. 2017 Feb;38(2):192-200.
[2]. Yang H, et al. Ginsenoside-Rb2and 20(S)-Ginsenoside-Rg3 from Koreanred ginseng prevent rotavirus infection in newborn mice. J Microbiol Biotechnol. 2018 Jan 11.
Ginsenoside Rc, one of major Ginsenosides from Panax ginseng, enhances GABA receptorA (GABAA)-mediated ion channel currents (IGABA). Ginsenoside Rc inhibits the expression of TNF-α and IL-1β.
IC50 Target[2]
TNF-α
;
IL-1β
;
体外研究 (In Vitro)
Ginsenoside Rc, one of major Ginsenosides from Panax ginseng, enhances γ-aminobutyric acid (GABA) receptorA (GABAA)-mediated ion channel currents. Ginsenoside Rc enhances GABA-mediated ion currents in oocytes expressing the GABAA receptor[1]. Ginsenoside Rc significantly inhibits the expression of macrophage-derived cytokines, such as TNF-α and IL-1β. Ginsenoside Rc also markedly suppresses the activation of TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling in activated RAW264.7 macrophages, human synovial cells, and HEK293 cells. Ginsenoside Rc exerts its anti-inflammatory actions by suppressing TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling. Ginsenoside Rc suppresses the nuclear translocation of phospho-ATF-2 and phospho-FRA-1, whereas the translocation of p65 at its peak time points (30 and 60 min) is not decreased by Ginsenoside Rc treatment. Ginsenoside Rc regulates the expression of the proinflammatory cytokine TNF-α, which is produced by macrophages, by suppressing AP-1 activation[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
1079.27
Formula
C53H90O22
CAS 号
11021-14-0
中文名称
人参皂苷 Rc
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Lee BH, et al. Effects of Ginsenoside Metabolites on GABAA Receptor-Mediated Ion Currents. J Ginseng Res. 2012 Jan;36(1):55-60.
[2]. Yu T, et al. Ginsenoside Rc from Panax ginseng exerts anti-inflammatory activity by targeting TANK-bindingkinase 1/interferon regulatory factor-3 and p38/ATF-2. J Ginseng Res. 2017 Apr;41(2):127-133.
Kinase Assay [2]
To evaluate the effects of Ginsenoside Rc on kinase activity, immunoprecipitated TBK1, IKKε, and p38 are incubated in reaction buffer in the presence or absence of Ginsenoside Rc. The reactions are initiated by the addition of Mg-ATP. After a 30 min incubation at 30°C, the reactions are stopped by the addition of sample buffer and the samples are boiled. Kinase activity is assessed by immunoblotting with antibodies against the phospho-forms of IKKε, IRF-3, and ATF-2[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Lee BH, et al. Effects of Ginsenoside Metabolites on GABAA Receptor-Mediated Ion Currents. J Ginseng Res. 2012 Jan;36(1):55-60.
[2]. Yu T, et al. Ginsenoside Rc from Panax ginseng exerts anti-inflammatory activity by targeting TANK-bindingkinase 1/interferon regulatory factor-3 and p38/ATF-2. J Ginseng Res. 2017 Apr;41(2):127-133.
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.
Ginsenoside Rf 是人参根的一种微量成分。 Ginsenoside Rf 抑制 N 型 Ca2+ 通道。
Ginsenoside Rf Chemical Structure
CAS No. : 52286-58-5
规格
价格
是否有货
数量
10;mM;*;1 mL in DMSO
￥1498
In-stock
5 mg
￥990
In-stock
10 mg
￥1700
In-stock
50 mg
;
询价
;
100 mg
;
询价
;
* Please select Quantity before adding items.
Ginsenoside Rf 相关产品
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生物活性
Ginsenoside Rf is a trace component of ginseng root. Ginsenoside Rf inhibits N-type Ca2+ channel.
IC50 Target[1]
N-Type Ca2+ Channel
;
Human Endogenous Metabolite
;
体外研究 (In Vitro)
Ginsenoside Rf is a saponin, which is present in only trace amounts within ginseng. At saturating concentrations, Ginsenoside Rf rapidly and reversibly inhibits N-type, and other high-threshold, Ca2+ channels in rat sensory neurons to the same degree as a maximal dose of opioids. The effect is dose-dependent (half-maximal inhibition: 40 μM) and it is virtually eliminated by pretreatment of the neurons with pertussis toxin, an inhibitor of G(o) and Gi GTP-binding proteins. Ginsenoside Rf also inhibits Ca2+ channels in the hybrid F-11 cell line[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Since inhibition of Ca2+ channels in sensory neurons contributes to antinociception by opioids, analgesic actions of Ginsenoside Rf are tested. Dose-dependent antinociception is found by systemic administration of Ginsenoside Rf in mice using two separate assays of tonic pain: in the acetic acid abdominal constriction test, the ED50 is 56±9 mg/kg, a concentration similar to those reported for aspirin and acetaminophen in the same assay; in the tonic phase of the biphasic formalin test, the ED50 is 129±32 mg/kg[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
801.01
Formula
C42H72O14
CAS 号
52286-58-5
中文名称
人参皂苷 Rf；人参皂苷 Rf
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Nah SY, et al. A trace component of ginseng that inhibits Ca2+ channels through a pertussis toxin-sensitive G protein. Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8739-43.
[2]. Mogil JS, et al. Ginsenoside Rf, a trace component of ginseng root, produces antinociception in mice. Brain Res. 1998 May 11;792(2):218-28.
Animal Administration [2]
Mice[2] Naive, adult (7-12 week old) mice of outbred Swiss-Webster stock are used in all in vivo experiments. Mice are brought to a quiet testing room, and acclimated to table-top Plexiglas observation chambers (30 cm high; 30 cm diameter) for 30 min. They are then weighed and injected with Ginsenoside Rf (25, 50, or 75 mg/kg) or vehicle (preceded by naloxone or saline in one experiment). Twenty min later, a 0.9% solution of glacial acetic acid is injected intraperitoneally (i.p.) in a volume of 10 mL/kg. For the next 30 min, the number of constrictions (writhes)-strong contractions of the abdominal musculature accompanied by dorsoflexion of the back and extension of the hindlimbs-are counted and recorded in 5-min blocks. Four mice (one per chamber) are observed simultaneously by a single, experienced experimenter. To control for the considerable circadian and other environmental variance accompanying this nociceptive assay, two vehicle controls are tested alongside two Ginsenoside Rf-administered mice in every experimental session[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Nah SY, et al. A trace component of ginseng that inhibits Ca2+ channels through a pertussis toxin-sensitive G protein. Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8739-43.
[2]. Mogil JS, et al. Ginsenoside Rf, a trace component of ginseng root, produces antinociception in mice. Brain Res. 1998 May 11;792(2):218-28.
