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protopanaxadiol/necrosis
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15 resultados
In vitro inhibitory effect of protopanaxadiol ginsenosides on tumor necrosis factor (TNF)-alpha production and its modulation by known TNF-alpha antagonists.
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Ginsenosides are the major principles of Panax ginseng C. A. Meyer (Araliaceae) used as a mild oriental folk medicine. In this report, we have examined the inhibitory potency of protopanaxadiol ginsenosides (PPDGs) such as Rb1, Rb2 and Rc, and their co-treatment effect with known tumor necrosis
Snailase preparation of ginsenoside M1 from protopanaxadiol-type ginsenoside and their protective effects against CCl4-induced chronic hepatotoxicity in mice.
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To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl(4))-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The
Protopanaxadiol and Protopanaxatriol-Type Saponins Ameliorate Glucose and Lipid Metabolism in Type 2 Diabetes Mellitus in High-Fat Diet/Streptozocin-Induced Mice.
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Ginsenoside is a major active component of ginseng, which exhibits various pharmacological properties such as hepatoprotection, tumor suppression and diabetes resistance. In this study, the anti-diabetic effects of protopanaxadiol (PPD) and protopanaxatriol (PPT)-type saponins were explored and
Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions.
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BACKGROUND
Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated
TRAIL pathway is associated with inhibition of colon cancer by protopanaxadiol.
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Among important components of American ginseng, protopanaxadiol (PPD) showed more active anticancer potential than other triterpenoid saponins. In this study, we determined the in vivo effects of PPD in a mouse cancer model first. Then, using human colorectal cancer cell lines, we observed
A ginseng saponin metabolite suppresses tumor necrosis factor-alpha-promoted metastasis by suppressing nuclear factor-kappaB signaling in murine colon cancer cells.
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SC-514, an inhibitor of IkappaB kinase beta (IKKbeta), blocked the TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB) as well as the TNF-alpha-promoted metastasis of murine colon adenocarcinoma cells. We investigated the effect of 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (M1),
Korean red ginseng extract prevents APAP-induced hepatotoxicity through metabolic enzyme regulation: the role of ginsenoside Rg3, a protopanaxadiol.
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BACKGROUND
Inappropriate use of acetaminophen (APAP) can lead to morbidity and mortality secondary to hepatic necrosis.
OBJECTIVE
We evaluated the beneficial effect and molecular mechanism of Korean red ginseng (KRG) on the APAP-mediated hepatotoxicity and identified a major component of KRG for
Glucocorticoid receptor agonist compound K regulates Dectin-1-dependent inflammatory signaling through inhibition of reactive oxygen species.
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OBJECTIVE
Compound K (C-K; 20-O-D-glucopyranosyl-20(S)-protopanaxadiol) is a functional ligand of the glucocorticoid receptor (GR) and regulates toll-like receptor-4-dependent inflammation. Here, the role of C-K in the regulation of zymosan-mediated inflammation was investigated in murine bone
Ginsenoside Rg3 Improves Recovery from Spinal Cord Injury in Rats via Suppression of Neuronal Apoptosis, Pro-Inflammatory Mediators, and Microglial Activation.
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Spinal cord injury (SCI) is one of the most devastating medical conditions; however, currently, there are no effective pharmacological interventions for SCI. Ginsenoside Rg3 (GRg3) is one of the protopanaxadiols that show anti-inflammatory, anti-oxidant, and neuroprotective effects. The present
Inhibition of TNF-α-mediated NF-κB Activation by Ginsenoside Rg1 Contributes the Attenuation of Cardiac Hypertrophy Induced by Abdominal Aorta Coarctation.
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Ginsenoside Rg1 (Rg1), a protopanaxadiol saponin extracted from Chinese medicine Panax ginseng C.A. Meyer, has been demonstrated to inhibit the cardiac hypertrophy. However, the molecular mechanisms underlying the inhibition remain poorly understood. Activation of nuclear factor-kappa B (NF-κB)
Comparative study on saponin fractions from Panax notoginseng inhibiting inflammation-induced endothelial adhesion molecule expression and monocyte adhesion.
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BACKGROUND
Panax notoginseng is commonly used for the treatment of cardiovascular diseases in China. The present study investigates the effects of three different saponin fractions (ie total saponins, PNS; protopanaxadiol-type saponin, PDS; and protopanaxatriol-type saponin, PTS) and two major
Ginsenoside Re ameliorates inflammation by inhibiting the binding of lipopolysaccharide to TLR4 on macrophages.
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Ginseng (the root of Panax ginseng C.A. Meyer, family Araliaceae), which contains protopanaxadiol ginsenoside Rb1 and protopanaxatriol ginsenoside Re as main constituents, is frequently used to treat cancer, inflammation, and stress. In the preliminary study, protopanaxatriol ginsenoside Re
Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation.
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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
Ginsenoside Rc from Panax ginseng exerts anti-inflammatory activity by targeting TANK-binding kinase 1/interferon regulatory factor-3 and p38/ATF-2.
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BACKGROUND
Ginsenoside Rc (G-Rc) is one of the major protopanaxadiol-type saponins isolated from Panax ginseng, a well-known medicinal herb with many beneficial properties including anticancer, anti-inflammatory, antiobesity, and antidiabetic effects. In this study, we investigated the effects of
Anti-inflammatory mechanism of compound K in activated microglia and its neuroprotective effect on experimental stroke in mice.
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Microglial activation plays a pivotal role in the pathogenesis of various neurologic disorders, such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. Thus, controlling microglial activation is a promising therapeutic strategy for such brain diseases. In the present study, we found
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