|Source:||The roots of Panax ginseng C. A. Mey.|
|Biological Activity or Inhibitors:||1. Ginsenoside Rh1 has antiallergic action, may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.
2. Ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.
3. Ginsenoside Rh1 can upregulate glucocorticoid receptor (GR) level, suggests Rh1 may improve glucocorticoid efficacy in hormone-dependent diseases, it may enhance the effect of Dex in the treatment of MRL/lpr mice through regulating CD4+ T cells activation and Th1/Th2 balance.
4. Ginsenoside Rh1 can inhibit 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, suggests that ginsenoside Rh1 may have a therapeutic potential for malignant gliomas.
5. Ginsenoside Rh1 inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression, thus, the inhibition of microglial activation by ginsenoside Rh1 may provide potential therapeutic strategy for various neuroinflammatory diseases.
6. Ginsenoside Rh1 has anti-inflammatory activity, 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.
|Solvent:||Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|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|
Neurochem Int. 2013 Aug;63(2):80-6.
|Protopanaxatriol ginsenoside Rh1 inhibits the expression of matrix metalloproteinases and the in vitro invasion/migration of human astroglioma cells.[Pubmed: 23684955 ]|
|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-κB 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.|
Biol Pharm Bull. 2013;36(1):102-7.
|Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation.[Pubmed: 23302642]|
|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)-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. Based on these findings, Ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.|
Biochem Biophys Res Commun. 2010 Jun 25;397(2):323-8.
|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]|
|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.|
Fitoterapia. 2011 Sep;82(6):911-9.
|Ginsenoside Rh1 inhibits the invasion and migration of THP-1 acute monocytic leukemia cells via inactivation of the MAPK signaling pathway.[Pubmed: 21605636]|
|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 β1 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.|
Int Arch Allergy Immunol. 2004 Feb;133(2):113-20.
|Ginsenoside Rh1 possesses antiallergic and anti-inflammatory activities.[Pubmed: 14739579 ]|
|Ginsenoside Rh1 (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.|
Evid Based Complement Alternat Med. 2015;2015:727650.
|Ginsenoside Rh1 Improves the Effect of Dexamethasone on Autoantibodies Production and Lymphoproliferation in MRL/lpr Mice.[Pubmed: 25918545 ]|
|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-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. 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.|