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 Rk3 is present in the roots Panax notoginseng herbs. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM in HepG2 cells.
IC50 Target[1]
NF-κB
14.24 mu;M (IC50, in HepG2 cells)
NF-κB
15.32 mu;M (IC50, in SK-Hep1 cell)
体外研究 (In Vitro)
Ginsenoside Rk3 exerts the strong activity inhibiting NF-κB in a dose-dependent manner. HepG2 cells are pre-treated with different ginsenosides at concentrations ranging from 0.01 to 10 μM for 1 h, and induced with TNF-α for 20 h. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 15.32±0.29 μM in SK-Hep1 cells, consistent with the data from HepG2 cells. Consistent with the inhibition of NF-κB, Ginsenoside Rk3 inhibits the induction of IL8, CXCL1, iNOS, and ICAM1 mRNA significantly in a dose-dependent manner[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
The inhibitory effects of Ginsenoside Rk3 (Rk3) on tumor progression are studied in vivo using a H460 xenograft model in nude mice. Compared with the control group, a significant inhibition of tumor growth (volume) is observed in the Ginsenoside Rk3-treated group. Twenty-one days after treatment initiation, tumor growth is significantly inhibited by approximately 62.99% in the mice receiving 20 mg/kg Ginsenoside Rk3, similar to the inhibitory effect observed in the 20 mg/kg Gefitinib-treated group (57.21%). Compared with the control group, tumor growth is moderately inhibited in the mice receiving 10 and 5 mg/kg Ginsenoside Rk3, with inhibition rates of 32.54% and 11.84%, respectively[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
620.86
Formula
C36H60O8
CAS 号
364779-15-7
中文名称
人参皂甙 Rk3
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]. Duan Z, et al. Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo. Food Funct. 2017 Oct 18;8(10):3723-3736.
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)-8 is used to analyze the effect of compounds (e.g., Ginsenoside Rk3; 0.01, 0.1, 1 and 10 uM) 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.
Animal Administration [2]
Mice[2] Four- to 5-week-old male nude mice are selected and housed under aseptic conditions. The animals are exposed to a phase shift of the light/dark cycle for one week and allowed free access to a normal diet. All animal handling is performed under a laminar flow hood. The H460 xenograft model is established. Cell suspensions at a density of 4-5×106 cells are subcutaneously implanted into the left axilla of each mouse. Tumor engraftment is considered successful when the tumors are clearly visible, which occurs after one to two weeks. The tumor-bearing mice are randomly divided into the following 5 groups (5 mice per group) according to tumor size and body weight: control group (0.9% saline solution), Ginsenoside Rk3-treated group (5/10/20 mg/kg), and Gefitinib-treated group (20 mg/kg). The indicated doses (5-20 mg/kg) of Ginsenoside Rk3 are safe for mice as determined by preliminary acute oral toxicity tests. The dose of Gefitinib is based on the results from another study. Mice are intragastrically treated daily for 21 days. The tumor volumes are estimated. The body weights and tumor volumes of the mice in each group are measured twice per week. After 21 days, all animals are euthanized, and all tumor tissues are removed, weighed, and collected.
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]. Duan Z, et al. Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo. Food Funct. 2017 Oct 18;8(10):3723-3736.