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Inhibition of inflammations and macrophage activation by ginsenoside-Re isolated from Korean ginseng (Panax ginseng C.A. Meyer).

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This study was undertaken to evaluate the effect of ginsenoside-Re (Gin-Re) isolated from roots of Panax ginseng on carrageenan-induced paw and TPA-induced skin inflammations in experimental mice. Moreover, to confirm further the anti-inflammatory activities of Gin-Re, LPS-induced macrophage

Effects of ginsenoside Re on LPS-induced inflammatory mediators in BV2 microglial cells.

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BACKGROUND Microglial activation plays an important role in neurodegenerative diseases by producing several pro-inflammatory enzymes and pro-inflammatory cytokines. Lipopolysaccharide (LPS)-induced inflammation leads to the activation of microglial cells in the central nervous system (CNS) and is

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

Altered expression of serum protein in ginsenoside Re-treated diabetic rats detected by SELDI-TOF MS.

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Diabetes mellitus (DM) is now a global health problem, however, its pathogenesis has not yet been fully deciphered. Even though modern medicine has great contribution to the control and treatment of DM, it is still far from success to completely cure the disease. Panax ginseng C.A. Meyer (ginseng)

Protective effects of ginsenoside Re on lipopolysaccharide-induced cardiac dysfunction in mice.

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The impaired cardiac function caused by reduced myocardial contractility is a typical manifestation of sepsis/septic shock. Ginsenoside Re (GS-Re) is one of the most abundant ingredients of ginseng. This study was designed to investigate the protective effects of GS-Re on lipopolysaccharide

Ginsenoside Rd and ginsenoside Re offer neuroprotection in a novel model of Parkinson's disease.

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Ginsenosides are the main active constituents of Panax ginseng. Ginsenoside Re is one of the major ginsenosides; whereas hydrolysis products such as Rd appear to have higher biological activity though are present in smaller amounts. Ginsenosides, from their early use in folk medicine to modern

Ginsenoside-Re ameliorates ischemia and reperfusion injury in the heart: a hemodynamics approach.

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Ginsenosides are divided into two groups based on the types of the panaxadiol group (e.g., ginsenoside-Rb1 and -Rc) and the panaxatriol group (e.g., ginsenoside-Rg1 and -Re). Among them, ginsenoside-Re (G-Re) is one of the compounds with the highest content in Panax ginseng and is responsible for

Kidney Protection Effect of Ginsenoside Re and Its Underlying Mechanisms on Cisplatin-Induced Kidney Injury.

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OBJECTIVE Cisplatin (CDDP) was the first platinum-containing anti-cancer drug. However, CDDP causes nephrotoxicity as a side effect, which limits its clinic application. The aim of this study was to investigate the renoprotective effect of ginsenoside Re (G-Re) in a murine model of CDDP-induced

Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor.

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BACKGROUND We previously reported that ginsenoside Re (GRe) attenuated against methamphetamine (MA)-induced neurotoxicity via anti-inflammatory and antioxidant potentials. We also demonstrated that dynorphin possesses anti-inflammatory and antioxidant potentials against dopaminergic loss, and that

Ginsenoside Re inhibits vascular neointimal hyperplasia in balloon-injured carotid arteries through activating the eNOS/NO/cGMP pathway in rats.

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Ginsenoside Re (GS-Re) is one of the main ingredients of ginseng, a widely known Chinese traditional medicine, and has a variety of beneficial effects, including vasorelaxation, antioxidative, anti-inflammatory, and anticancer properties. The aims of the present study were to observe the effect of

Ginsenoside Re Attenuates High Glucose-Induced RF/6A Injury via Regulating PI3K/AKT Inhibited HIF-1α/VEGF Signaling Pathway

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Hyperglycaemia-induced retinal microvascular endothelial cell apoptosis is a critical and principle event in diabetic retinopathy (DR), which involves a series of complex processes such as mitochondrial dysfunction and oxidative stress. Ginsenoside Re (Re), a key ingredients of ginseng, is

Microbial transformation of ginsenoside Rb1, Re and Rg1 and its contribution to the improved anti-inflammatory activity of ginseng.

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Microbial transformation of ginsenosides to increase its pharmaceutical effect is gaining increasing attention in recent years. In this study, Cellulosimicrobium sp. TH-20, which was isolated from soil samples on which ginseng grown, exhibited effective ginsenoside-transforming activity. After

Salvianolic Acid B and Ginsenoside Re Synergistically Protect Against Ox-LDL-Induced Endothelial Apoptosis Through the Antioxidative and Antiinflammatory Mechanisms.

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Salvianolic acid B (SalB) and ginsenoside Re (Re) protect endotheliocytes against apoptosis through different mechanisms. However, whether both compounds could synergistically protect endothelial cells against oxidized low-density lipoprotein (Ox-LDL)-induced apoptosis is unclear. This study aimed

Ginseng Berry Prevents Alcohol-Induced Liver Damage by Improving the Anti-Inflammatory System Damage in Mice and Quality Control of Active Compounds.

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The ginseng berry contains a variety of biologically active compounds and has a higher ginsenoside content than its roots. This study focused on the hepatoprotective activity of ginseng berry extract prepared by enzyme treatment (EGB) compared to the non-enzyme-treated ginseng berry extract (GB) and

Ginsenoside Re attenuates diabetes-associated cognitive deficits in rats.

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OBJECTIVE This study was designed to investigate the effect of ginsenoside Re (Re) on cognitive functions, oxidative stress and inflammation in streptozotocin-induced diabetic rats. METHODS Diabetic rats were treated with Re (40mg/kg) for 8weeks, blood glucose and body weight were measured monthly

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