Notoginsenoside R1(NR1) is the main ingredient with cardiovascular activity in Panax notoginseng, which has some neuronal protective, antihypertensive,antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. NR1 can counteract endotoxin-induced activation of endothelial cells in vitro and endotoxin-induced lethality in mice in vivo. NR1 inhibits TNF-α-induced PAI-1 overexpression via extracellular signal-related kinases (ERK1/2) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling pathways, it attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation.
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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.
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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.
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Arterioscler Thromb Vasc Biol. 1997 Mar;17(3):465-74.
Notoginsenoside R1 counteracts endotoxin-induced activation of endothelial cells in vitro and endotoxin-induced lethality in mice in vivo.[Pubmed: 9102164
In this study we investigated a possible counteracting activity Notoginsenoside R1 (NG-R1) on lipopolysaccharide (LPS)-induced effects in vitro and in vivo.
METHODS AND RESULTS:
The upregulation of plasminogen activator inhibitor-1 (PAI-1) antigen due to LPS (1 microgram/mL for 12 hours) in human umbilical vein endothelial cells (HUVECs) was prevented when the cells were incubated simultaneously with 100 micrograms/mL NG-R1 (PAI-1 antigen: LPS-treated cells, 969 +/- 54 ng/10(5) cells; control cells, 370 +/- 15 ng/10(5) cells; LPS + NG-R1-treated cells, 469 +/- 29 ng/10(5) cells; n = 6). The 2.5- and 3.4-fold (2.2- and 3.2-kb) increases in PAI-1 mRNA levels induced by LPS (1 microgram/mL for 6 hours) were reduced to 1.4- and 2.6-fold increases in the presence of both LPS and 100 micrograms/mL NG-R1. LPS-induced tissue factor (TF) activity in HUVECs was also counteracted when the cells were coincubated with both LPS and 100 micrograms/mL NG-R1 for 6 hours (TF activity: LPS-treated cells, 88.6 +/- 6.5 mU/10(6) cells; control cells, 0.7 +/- 0.01 mU/10(6) cells; LPS + NG-R1-treated cells, 56.0 +/- 1.9 mU/10(6) cells). The 26-fold increase in TF mRNA levels induced by LPS (1 microgram/mL for 2 hours) was reduced to a 13-fold increase in the presence of both LPS and 100 micrograms/mL NG-R1. PAI activity levels in the plasma of mice 4 hours after injection of LPS (10 ng/g body wt) increased 2.3-fold compared with a control group. In contrast, PAI activity from LPS + NG-R1 (1 microgram/g body wt NG-R1)-treated animals was at control level (PAI-1 activity: LPS-treated group, 11.3 +/- 3.1 U/mL; control group, 4.9 +/- 0.3 U/mL; LPS + NG-R1-treated group, 4.3 +/- 1.0 U/mL; n = 5 to 8). The production of TNF-alpha induced by 1 microgram/mL LPS by cultured human whole-blood cells was inhibited by 46% when the cells were incubated together with 100 micrograms/mL NG-R1. NG-R1 protected mice from the lethal effects of LPS. The 78% lethality induced by LPS/galactosamine was reduced to 23% when NG-R1 was administered simultaneously (P < .01 by chi 2 test).
To extend this study to inflammatory cells, the effect of NG-R1 on LPS stimulation of the monocytic cell line THP-1 was investigated.
NG-R1 inhibited the LPS-induced degradation of I kappa B-alpha and superinduced LPS-induced I kappa B-alpha mRNA, indicating that the effect of NG-R1 is not restricted to endothelial cells and is at least in part mediated by interference with the NF-kappa B/I kappa B-alpha pathway.
Int Immunopharmacol. 2014 Sep;22(1):151-9.
Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation.[Pubmed: 24975829
Progressive accumulation of amyloid-β (Aβ) is a pathological hallmark of Alzheimer's disease (AD). Aβ increases free radical production in neuronal cells, leading to oxidative stress and cell death.
METHODS AND RESULTS:
An intervention that would reduce Aβ-related neurotoxicity through free radical reduction could advance the treatment of AD. Notoginsenoside R1 (NR1), the major and most active ingredient in the herb Panax notoginseng, can reduce reactive oxygen species and confer some neuroprotective effects. Here, NR1 was applied in a cell-based model of Alzheimer's disease. Cell viability, cell death, reactive oxygen species generation, and mitochondrial membrane potential were assessed in cultured PC12 neuronal cells incubated with Aβ(25-35). In this model, Aβ was neurotoxic and induced necrosis and apoptosis; however, NR1 significantly counteracted the effects of Aβ by increasing cell viability, reducing oxidative damage (including apoptosis), restoring mitochondrial membrane potential, and suppressing stress-activated MAPK signaling pathways.
These results promise a great potential agent for Alzheimer's disease and other Aβ pathology-related neuronal degenerative disease.
Free Radic Biol Med. 2006 May 1;40(9):1664-74.
Notoginsenoside R1 inhibits TNF-alpha-induced fibronectin production in smooth muscle cells via the ROS/ERK pathway.[Pubmed: 16632126
The matrix fibronectin protein plays an important role in vascular remodeling. Notoginsenoside R1 is the main ingredient with cardiovascular activity in Panax notoginseng; however, its molecular mechanisms are poorly understood.
METHODS AND RESULTS:
We report that Notoginsenoside R1 significantly decreased TNF-alpha-induced activation of fibronectin mRNA, protein levels, and secretion in human arterial smooth muscle cells (HASMCs) in a dose-dependent manner. Notoginsenoside R1 scavenged hydrogen peroxide (H2O2) in a dose-dependent manner in the test tube. TNF-alpha significantly increased intracellular ROS generation and then ERK activation, which was blocked by Notoginsenoside R1 or DPI and apocynin, inhibitors of NADPH oxidase, or the antioxidant NAC. Our data demonstrated that TNF-alpha-induced upregulation of fibronectin mRNA and protein levels occurs via activation of ROS/ERK, which was prevented by treatment with Notoginsenoside R1, DPI, apocynin, NAC, or MAPK/ERK inhibitors PD098059 and U0126. Notoginsenoside R1 significantly inhibited H2O2-induced upregulation of fibronectin mRNA and protein levels and secretion; it also significantly inhibited TNF-alpha and H2O2-induced migration.
These results suggest that Notoginsenoside R1 inhibits TNF-alpha-induced ERK activation and subsequent fibronectin overexpression and migration in HASMCs by suppressing NADPH oxidase-mediated ROS generation and directly scavenging ROS.
J Neurosci Res. 2009 Jul;87(9):2145-56.
Possible protection by notoginsenoside R1 against glutamate neurotoxicity mediated by N-methyl-D-aspartate receptors composed of an NR1/NR2B subunit assembly.[Pubmed: 19224577
Notoginsenoside R1 (NTR1) is the main active ingredient in Panax notoginseng, a herbal medicine widely used in Asia for years. The purpose of this study was to investigate pharmacological properties of NTR1 on neurotoxicity of glutamate (Glu) in primary cultured mouse cortical neurons along with its possible mechanism of action.
METHODS AND RESULTS:
We found that NTR1 significantly protected neurons from the loss of cellular viability caused by brief exposure to 10 microM Glu for 1 hr in a dose-dependent manner at concentrations from 0.1 to 10 microM, without affecting the viability alone. NTR1 significantly inhibited the increased number of cells positive to propidium iodide (PI) staining, increase of intracellular free Ca(2+) ions, overproduction of intracellular reactive oxygen species, and depolarization of mitochondrial membrane potential in cultured neurons exposed to Glu, in addition to blocking decreased Bcl-2 and increased Bax expression levels. We further evaluated the target site at which NTR1 protects neurons from Glu toxicity by using the acquired expression strategy of N-methyl-D-aspartate (NMDA) receptor subunits in human embryonic kidney 293 cells. We found that 10 microM NTR1 protected NR1/NR2B subunit expressing cells from cell death by 100 microM NMDA, but not cells expressing NR1/NR2A subunits, when determined by PI staining.
These results suggest that NTR1 may preferentially protect neurons from Glu excitotoxicity mediated by NMDA receptor composed of an NR1/NR2B subunit assembly in the brain.
Shock. 2010 Sep;34(3):314-20.
Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats.[Pubmed: 20023602
Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, Notoginsenoside R1(NR1) has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury.
METHODS AND RESULTS:
Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg.kg.d) and NR1-2 group (rats treated with NR1, 40 mg.kg.d). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-alpha, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor kappaB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2.
Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor kappaB inhibition.