Ginsenoside Rh1

CAS# 63223-86-9

Ginsenoside Rh1

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Chemical structure

Ginsenoside Rh1

3D structure

Chemical Properties of Ginsenoside Rh1

Cas No. 63223-86-9 SDF Download SDF
PubChem ID 3085260 Appearance White powder
Formula C36H62O9 M.Wt 638.88
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms Prosapogenin A2; Sanchinoside B2; Sanchinoside Rh1; Ginsenoside-Rh1
Solubility DMSO : 100 mg/mL (156.53 mM; Need ultrasonic)
Chemical Name (2R,3R,4S,5S,6R)-2-[[(3S,5R,6S,8R,10R,12R,14R,17S)-3,12-dihydroxy-17-[(2S)-2-hydroxy-6-methylhept-5-en-2-yl]-4,4,8,10,14-pentamethyl-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-6-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol
SMILES CC(=CCCC(C)(C1CCC2(C1C(CC3C2(CC(C4C3(CCC(C4(C)C)O)C)OC5C(C(C(C(O5)CO)O)O)O)C)O)C)O)C
Standard InChIKey RAQNTCRNSXYLAH-YFEBDHGLSA-N
Standard InChI InChI=1S/C36H62O9/c1-19(2)10-9-13-36(8,43)20-11-15-34(6)26(20)21(38)16-24-33(5)14-12-25(39)32(3,4)30(33)22(17-35(24,34)7)44-31-29(42)28(41)27(40)23(18-37)45-31/h10,20-31,37-43H,9,11-18H2,1-8H3/t20-,21+,22-,23+,24?,25-,26?,27+,28-,29+,30-,31+,33+,34+,35+,36-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Ginsenoside Rh1

The roots of Panax ginseng C. A. Mey.

Biological Activity of Ginsenoside Rh1

DescriptionGinsenoside Rh1 has anti-obesity, anti-inflammatory, antiallergic, and anti-tumor activities, it may improve glucocorticoid efficacy in hormone-dependent diseases. It inhibits MAPK and PI3K/Akt signaling pathways and downstream transcription factors such as NF-κB and AP-1, which play an important role in MMP gene expressions; it also inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression.
TargetsMMP(e.g.TIMP) | MAPK | PI3K | Akt | NF-kB | AP-1 | PPAR | IL Receptor | TNF-α | NOS | NO | IFN-γ | STAT | JAK | ERK | COX | gp120/CD4
In vitro

Protopanaxatriol ginsenoside Rh1 inhibits the expression of matrix metalloproteinases and the in vitro invasion/migration of human astroglioma cells.[Pubmed: 23684955 ]

Neurochem Int. 2013 Aug;63(2):80-6.

Malignant gliomas are the most common and fatal brain tumors in adults. In particular, the strong invasiveness of glioma cells into the normal brain tissue makes eradication of glioma very difficult. Matrix metalloproteinases (MMPs) play a pivotal role in glioma invasion, and thus controlling MMP expression has been suggested as an important therapeutic target for brain tumors. In the present study, we investigated the effect of protopanaxatriol Ginsenoside Rh1 on MMP expressions in human astroglioma U87MG and U373MG cells.
METHODS AND RESULTS:
RT-PCR analysis showed that Rh1 inhibits the mRNA expressions of MMP-1, -3, and -9 in PMA-stimulated U87MG and U373MG cells. Rh1 also suppressed the promoter activities of MMP-1, -3 and -9. The ELISA, Western blot, and zymographic analyses revealed that Rh1 inhibits the protein expression and/or enzymatic activity of MMP-1, -3 and -9. In accordance with the strong inhibitory effects of Rh1 on MMPs, Rh1 efficiently inhibited the invasion and migration of U87MG and U373MG glioma cells as demonstrated by Matrigel invasion assay and wound healing assay. Further mechanistic studies revealed that Rh1 inhibits MAPK and PI3K/Akt signaling pathways and downstream transcription factors such as NF-κB and AP-1, which play an important role in MMP gene expressions.
CONCLUSIONS:
The data collectively suggest that Ginsenoside Rh1 may have a therapeutic potential for malignant gliomas.

Ginsenoside Rh1 inhibits the invasion and migration of THP-1 acute monocytic leukemia cells via inactivation of the MAPK signaling pathway.[Pubmed: 21605636]

Fitoterapia. 2011 Sep;82(6):911-9.

Ginsenoside Rh1 has been reported to possess antiallergic and anti-inflammatory activities, but its effects on monocytes remain to be determined.
METHODS AND RESULTS:
Herein, we investigated the effects of Rh1 on the expression of MCP-1 and CCR2, activation of MAPK signaling, and chemotaxis of monocytes. Treatment of Rh1 decreased the levels of MCP-1 and CCR2 and the expression of VLA5 and activated β1 integrin on the cell surface, and attenuated the phosphorylation of MAPKs.
CONCLUSIONS:
Based on these results, the inhibitory effects of Rh1 on monocyte function should be regarded as a promising new anti-inflammatory response with a potential therapeutic role against inflammation-dependent diseases.

In vivo

Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation.[Pubmed: 23302642]

Biol Pharm Bull. 2013;36(1):102-7.

Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol Ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice.
METHODS AND RESULTS:
Treatment with Ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that Ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of Ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis.
CONCLUSIONS:
Based on these findings, Ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.

Ginsenoside Rh1 possesses antiallergic and anti-inflammatory activities.[Pubmed: 14739579 ]

Int Arch Allergy Immunol. 2004 Feb;133(2):113-20.

Ginseng (the root of Panax ginseng C.A. Meyer, Araliaceae) has been reported to possess various biological activities, including anti-inflammatory and antitumor actions. In this study, we investigated the antiallergic activity of ginsenosides isolated from ginseng.
METHODS AND RESULTS:
We isolated ginsenosides by silica gel column chromatography and examined their in vitro and in vivo antiallergic effect on rat peritoneal mast cells and on IgE-induced passive cutaneous anaphylaxis (PCA) in mice. The in vitro anti-inflammatory activity of Ginsenoside Rh1 (Rh1) in RAW264.7 cells was investigated. Rh1 potently inhibited histamine release from rat peritoneal mast cells and the IgE-mediated PCA reaction in mice. The inhibitory activity of Rh1 (87% inhibition at 25 mg/kg) on the PCA reaction was found to be more potent than that of disodium cromoglycate (31% inhibition at 25 mg/kg); Rh1 was also found to have a membrane-stabilizing action as revealed by differential scanning calorimetry. It also inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression in RAW 264.7 cells, and the activation of the transcription factor, NF-kappaB, in nuclear fractions.
CONCLUSIONS:
The antiallergic action of Rh1 may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies. CONCLUSION: The antiallergic action of Rh1 may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.

Protocol of Ginsenoside Rh1

Cell Research

Ginsenoside Rh1 suppresses inducible nitric oxide synthase gene expression in IFN-gamma-stimulated microglia via modulation of JAK/STAT and ERK signaling pathways.[Pubmed: 20510882]

Biochem Biophys Res Commun. 2010 Jun 25;397(2):323-8.

Microglial activation plays an important role in the pathogenesis of various neurodegenerative diseases by producing neurotoxic factors, such as pro-inflammatory cytokines and nitric oxide (NO). In the present study, we found that protopanaxatriol Ginsenoside Rh1 suppresses NO, ROS, and TNF-alpha production in IFN-gamma-stimulated BV2 microglial cells. Rh1 inhibited the mRNA and protein expression of iNOS and TNF-alpha.
METHODS AND RESULTS:
To determine the regulatory mechanism of iNOS gene expression by Rh1, promoter analysis was performed. Rh1 significantly suppressed IFN-gamma-induced iNOS promoter activity by inhibiting DNA binding of several transcription factors, such as NF-kappaB, IRF-1, and STAT1. Furthermore, Rh1 inhibited the phosphorylation of JAK1, STAT1, STAT3, and ERK, which are upstream signaling molecules for IFN-gamma-induced iNOS gene expression. The present study demonstrates that Rh1 inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression.
CONCLUSIONS:
Therefore, the inhibition of microglial activation by Ginsenoside Rh1 may provide potential therapeutic strategy for various neuroinflammatory diseases.

Animal Research

Ginsenoside Rh1 Improves the Effect of Dexamethasone on Autoantibodies Production and Lymphoproliferation in MRL/lpr Mice.[Pubmed: 25918545 ]

Evid Based Complement Alternat Med. 2015;2015:727650.

Ginsenoside Rh1 is able to upregulate glucocorticoid receptor (GR) level, suggesting Rh1 may improve glucocorticoid efficacy in hormone-dependent diseases. Therefore, we investigated whether Rh1 could enhance the effect of dexamethasone (Dex) in the treatment of MRL/lpr mice.
METHODS AND RESULTS:
MRL/lpr mice were treated with vehicle, Dex, Rh1, or Dex + Rh1 for 4 weeks. Dex significantly reduced the proteinuria and anti-dsDNA and anti-ANA autoantibodies. The levels of proteinuria and anti-dsDNA and anti-ANA autoantibodies were further decreased in Dex + Rh1 group. Dex, Rh1, or Dex + Rh1 did not alter the proportion of CD4+ splenic lymphocytes, whereas the proportion of CD8+ splenic lymphocytes was significantly increased in Dex and Dex + Rh1 groups. Dex + Rh1 significantly decreased the ratio of CD4+/CD8+ splenic lymphocytes compared with control. Con A-induced CD4+ splenic lymphocytes proliferation was increased in Dex-treated mice and was inhibited in Dex + Rh1-treated mice. Th1 cytokine IFN-γ mRNA was suppressed and Th2 cytokine IL-4 mRNA was increased by Dex. The effect of Dex on IFN-γ and IL-4 mRNA was enhanced by Rh1.
CONCLUSIONS:
In conclusion, our data suggest that Rh1 may enhance the effect of Dex in the treatment of MRL/lpr mice through regulating CD4+ T cells activation and Th1/Th2 balance.

Ginsenoside Rh1 Dilution Calculator

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Preparing Stock Solutions of Ginsenoside Rh1

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.5652 mL 7.8262 mL 15.6524 mL 31.3048 mL 39.131 mL
5 mM 0.313 mL 1.5652 mL 3.1305 mL 6.261 mL 7.8262 mL
10 mM 0.1565 mL 0.7826 mL 1.5652 mL 3.1305 mL 3.9131 mL
50 mM 0.0313 mL 0.1565 mL 0.313 mL 0.6261 mL 0.7826 mL
100 mM 0.0157 mL 0.0783 mL 0.1565 mL 0.313 mL 0.3913 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Ginsenoside Rh1

Ginsenoside Rh1 is isolated from the root of Panax Ginseng. Ginsenoside Rh1 inhibits the expression of PPAR-γ, TNF-α, IL-6, and IL-1β.

In Vitro:The effect of Ginsenoside Rh1 is examined on adipogenesis in 3T3-L1 cells. Ginsenoside Rh1 potently inhibits the adipogenesis, as assessed by Oil-red O staining and lipid contents in 3T3-L1 adipocytes. Ginsenoside Rh1, at concentrations of 50 μM and 100 μM, inhibit the adipogenesis by 50% and 63%, respectively.The expression levels of adipocytespecific genes such as PPAR-γ, C/EBP-α, FAS, aFABP and some genes are examined during early phase of differentiation such as Pref-1, C/EBP-δ and Glucocorticoid receptor (GR). After the treatment with Ginsenoside Rh1 in 3T3-L1 cells, mRNA is extracted on 18 h and 24 h for Pref-1, C/EBP-δ and GR and day 8 for PPAR-γ, C/EBP-α, FAS, aFABP. Then, the expression profiles of adipocyte-specific genes are investigated by RT-PCR. PPAR-γ, C/EBP-α, FAS, and aFABP expressions are significantly increased in DMI-stimulated differentiated adipocyte compared to those of non-stimulated adipocyte cells. However, treatment with DMI in the presence of Ginsenoside Rh1 significantly suppresses the expression levels of PPAR-γ, C/EBP-α, FAS, and aFABP in a dose- dependent manner, whereas the expression levels of Pref-1, C/EBP-δ and GR are not affected[1].

In Vivo:When high-fat diet (HFD) fed mice for 8 weeks, body and epididymal fat weight gains are significantly increased compared to those of low-fat diet (LFD)-fed mice. However, when Ginsenoside Rh1 is treated in HFD-fed mice, body and epididymal fat weight gains are significantly decrease compared with those of the HFD-fed mice. TG, glucose, insulin, total cholesterol, and HDL levels in the blood are significantly increased in HFD-fed mice group compared to LFD-fed mice group. Treatment with Ginsenoside Rh1 in HFD-fed mice significantly lowers TG level alone[1].

References:
[1]. Gu W, et al. Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation. Biol Pharm Bull. 2013;36(1):102-7.

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References on Ginsenoside Rh1

Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation.[Pubmed:23302642]

Biol Pharm Bull. 2013;36(1):102-7.

Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol Ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with Ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that Ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-gamma, CCAAT/enhancer-binding protein (C/EBP)-alpha, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of Ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-gamma, C/EBP-alpha, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-1beta in DIO mice by real time PCR analysis. Based on these findings, Ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.

Ginsenoside Rh1 suppresses inducible nitric oxide synthase gene expression in IFN-gamma-stimulated microglia via modulation of JAK/STAT and ERK signaling pathways.[Pubmed:20510882]

Biochem Biophys Res Commun. 2010 Jun 25;397(2):323-8.

Microglial activation plays an important role in the pathogenesis of various neurodegenerative diseases by producing neurotoxic factors, such as pro-inflammatory cytokines and nitric oxide (NO). In the present study, we found that protopanaxatriol Ginsenoside Rh1 suppresses NO, ROS, and TNF-alpha production in IFN-gamma-stimulated BV2 microglial cells. Rh1 inhibited the mRNA and protein expression of iNOS and TNF-alpha. To determine the regulatory mechanism of iNOS gene expression by Rh1, promoter analysis was performed. Rh1 significantly suppressed IFN-gamma-induced iNOS promoter activity by inhibiting DNA binding of several transcription factors, such as NF-kappaB, IRF-1, and STAT1. Furthermore, Rh1 inhibited the phosphorylation of JAK1, STAT1, STAT3, and ERK, which are upstream signaling molecules for IFN-gamma-induced iNOS gene expression. The present study demonstrates that Rh1 inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression. Therefore, the inhibition of microglial activation by Ginsenoside Rh1 may provide potential therapeutic strategy for various neuroinflammatory diseases.

Ginsenoside Rh1 inhibits the invasion and migration of THP-1 acute monocytic leukemia cells via inactivation of the MAPK signaling pathway.[Pubmed:21605636]

Fitoterapia. 2011 Sep;82(6):911-9.

Ginsenoside Rh1 has been reported to possess antiallergic and anti-inflammatory activities, but its effects on monocytes remain to be determined. Herein, we investigated the effects of Rh1 on the expression of MCP-1 and CCR2, activation of MAPK signaling, and chemotaxis of monocytes. Treatment of Rh1 decreased the levels of MCP-1 and CCR2 and the expression of VLA5 and activated beta1 integrin on the cell surface, and attenuated the phosphorylation of MAPKs. Based on these results, the inhibitory effects of Rh1 on monocyte function should be regarded as a promising new anti-inflammatory response with a potential therapeutic role against inflammation-dependent diseases.

Ginsenoside Rh1 possesses antiallergic and anti-inflammatory activities.[Pubmed:14739579]

Int Arch Allergy Immunol. 2004 Feb;133(2):113-20.

BACKGROUND: Ginseng (the root of Panax ginseng C.A. Meyer, Araliaceae) has been reported to possess various biological activities, including anti-inflammatory and antitumor actions. In this study, we investigated the antiallergic activity of ginsenosides isolated from ginseng. METHOD: We isolated ginsenosides by silica gel column chromatography and examined their in vitro and in vivo antiallergic effect on rat peritoneal mast cells and on IgE-induced passive cutaneous anaphylaxis (PCA) in mice. The in vitro anti-inflammatory activity of Ginsenoside Rh1 (Rh1) in RAW264.7 cells was investigated. RESULTS: Rh1 potently inhibited histamine release from rat peritoneal mast cells and the IgE-mediated PCA reaction in mice. The inhibitory activity of Rh1 (87% inhibition at 25 mg/kg) on the PCA reaction was found to be more potent than that of disodium cromoglycate (31% inhibition at 25 mg/kg); Rh1 was also found to have a membrane-stabilizing action as revealed by differential scanning calorimetry. It also inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression in RAW 264.7 cells, and the activation of the transcription factor, NF-kappaB, in nuclear fractions. CONCLUSION: The antiallergic action of Rh1 may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.

Protopanaxatriol ginsenoside Rh1 inhibits the expression of matrix metalloproteinases and the in vitro invasion/migration of human astroglioma cells.[Pubmed:23684955]

Neurochem Int. 2013 Aug;63(2):80-6.

Malignant gliomas are the most common and fatal brain tumors in adults. In particular, the strong invasiveness of glioma cells into the normal brain tissue makes eradication of glioma very difficult. Matrix metalloproteinases (MMPs) play a pivotal role in glioma invasion, and thus controlling MMP expression has been suggested as an important therapeutic target for brain tumors. In the present study, we investigated the effect of protopanaxatriol Ginsenoside Rh1 on MMP expressions in human astroglioma U87MG and U373MG cells. RT-PCR analysis showed that Rh1 inhibits the mRNA expressions of MMP-1, -3, and -9 in PMA-stimulated U87MG and U373MG cells. Rh1 also suppressed the promoter activities of MMP-1, -3 and -9. The ELISA, Western blot, and zymographic analyses revealed that Rh1 inhibits the protein expression and/or enzymatic activity of MMP-1, -3 and -9. In accordance with the strong inhibitory effects of Rh1 on MMPs, Rh1 efficiently inhibited the invasion and migration of U87MG and U373MG glioma cells as demonstrated by Matrigel invasion assay and wound healing assay. Further mechanistic studies revealed that Rh1 inhibits MAPK and PI3K/Akt signaling pathways and downstream transcription factors such as NF-kappaB and AP-1, which play an important role in MMP gene expressions. The data collectively suggest that Ginsenoside Rh1 may have a therapeutic potential for malignant gliomas.

Ginsenoside Rh1 Improves the Effect of Dexamethasone on Autoantibodies Production and Lymphoproliferation in MRL/lpr Mice.[Pubmed:25918545]

Evid Based Complement Alternat Med. 2015;2015:727650.

Ginsenoside Rh1 is able to upregulate glucocorticoid receptor (GR) level, suggesting Rh1 may improve glucocorticoid efficacy in hormone-dependent diseases. Therefore, we investigated whether Rh1 could enhance the effect of dexamethasone (Dex) in the treatment of MRL/lpr mice. MRL/lpr mice were treated with vehicle, Dex, Rh1, or Dex + Rh1 for 4 weeks. Dex significantly reduced the proteinuria and anti-dsDNA and anti-ANA autoantibodies. The levels of proteinuria and anti-dsDNA and anti-ANA autoantibodies were further decreased in Dex + Rh1 group. Dex, Rh1, or Dex + Rh1 did not alter the proportion of CD4+ splenic lymphocytes, whereas the proportion of CD8+ splenic lymphocytes was significantly increased in Dex and Dex + Rh1 groups. Dex + Rh1 significantly decreased the ratio of CD4+/CD8+ splenic lymphocytes compared with control. Con A-induced CD4+ splenic lymphocytes proliferation was increased in Dex-treated mice and was inhibited in Dex + Rh1-treated mice. Th1 cytokine IFN-gamma mRNA was suppressed and Th2 cytokine IL-4 mRNA was increased by Dex. The effect of Dex on IFN-gamma and IL-4 mRNA was enhanced by Rh1. In conclusion, our data suggest that Rh1 may enhance the effect of Dex in the treatment of MRL/lpr mice through regulating CD4+ T cells activation and Th1/Th2 balance.

Description

Ginsenoside Rh1 (Prosapogenin A2; Sanchinoside B2; Sanchinoside Rh1) is isolated from the root of Panax Ginseng. Ginsenoside Rh1 inhibits the expression of PPAR-γ, TNF-α, IL-6, and IL-1β.

Keywords:

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