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Inhibitory effect of ginsenoside-Rd on carrageenan-induced inflammation in rats.

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A previous study reported that ginsenoside-Rd reduced the production of tumor necrosis factor-α by inhibiting nuclear factor-κB in lipopolysaccharide-activated N9 microglia in vitro. The aim of the present study was to confirm the anti-inflammatory effects and mechanisms of ginsenoside-Rd in animal

Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats.

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We previously found that ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, attenuates neuronal oxidative damage in vitro induced by hydrogen peroxide and oxygen-glucose deprivation. In this study, we sought to investigate the potential protective effects and associated

Ginsenoside-Rd exhibits anti-inflammatory activities through elevation of antioxidant enzyme activities and inhibition of JNK and ERK activation in vivo.

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Our previous study has reported that ginsenoside-Rd significantly inhibited the production of pro-inflammatory cytokines and mediators in carrageenan (Carr)-induced rat paw edema, which might be due to its blocking of the nuclear factor-κB (NF-κB) signaling pathway. The aim of the present study was

Ginsenoside Rd Is Efficacious Against Acute Ischemic Stroke by Suppressing Microglial Proteasome-Mediated Inflammation.

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A great deal of attention has been paid to neuroprotective therapies for cerebral ischemic stroke. Our two recent clinical trials showed that ginsenoside Rd (Rd), a kind of monomeric compound extracted from Chinese herbs, Panax ginseng and Panax notoginseng, was safe and efficacious for the

Ginsenoside Rd attenuates the inflammatory response via modulating p38 and JNK signaling pathways in rats with TNBS-induced relapsing colitis.

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In this study, we investigated the effects and the protective mechanism of ginsenoside Rd (GRd) which has been identified as one of the effective compounds from ginseng on relapsing colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats. After inducing relapsing colitis in

Ginsenoside Rd therapy improves histological and functional recovery in a rat model of inflammatory bowel disease

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Ginsenoside Rd (GRd) is a biologically active component of ginseng that stimulates the proliferation of endogenous stem cells. The objective of our research was to evaluate the utility of GRd in gastrointestinal mucosal regeneration in a rat model of inflammatory bowel disease (IBD) and to clarify

Ginsenoside Rd inhibits IL-1β-induced inflammation and degradation of intervertebral disc chondrocytes by increasing IL1RAP ubiquitination.

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Many compounds of ginsenosides show anti-inflammatory properties. However, their anti-inflammatory effects in intervertebral chondrocytes in the presence of inflammatory factors have never been shown. Increased levels of pro-inflammatory cytokines are generally associated with the degradation and

Retraction notice for: "Ginsenoside Rd inhibits IL-1β-induced inflammation and degradation of intervertebral disc chondrocytes by increasing IL1RAP ubiquitination" [Braz J Med Biol Res (2019) 52(9): e8525].

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[This retracts the article doi: 10.1590/1414-431x20198525].

Ginsenoside Rd contributes the attenuation of cardiac hypertrophy in vivo and in vitro.

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Cardiac hypertrophy are the major health challenges in the whole world. Ginsenoside Rd is an important component of cell growth and tumorigenesis, but the role and mechanism of ginsenoside Rd in pressure overload induced cardiac dysfunction and remodeling are still not fully illuminated. Here,

Ginsenoside Rd blocks AIF mitochondrio-nuclear translocation and NF-κB nuclear accumulation by inhibiting poly(ADP-ribose) polymerase-1 after focal cerebral ischemia in rats.

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Our previous clinical and basic studies have demonstrated that ginsenoside Rd (GS-Rd) has remarkable neuroprotective effects after cerebral ischemia but the underlying mechanisms are still unknown. In our latest studies, we revealed that GS-Rd could prevent mitochondrial release of

Ginsenoside Rd maintains adult neural stem cell proliferation during lead-impaired neurogenesis.

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Lead exposure attracts a great deal of public attention due to its harmful effects on human health. Even low-level lead (Pb) exposure reduces the capacity for neurogenesis. It is well known that microglia-mediated neurotoxicity can impair neurogenesis. Despite this, few in vivo studies have been

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 Rd reverses cognitive deficits by modulating BDNF-dependent CREB pathway in chronic restraint stress mice

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Cognitive impairment has been widely recognized as a common symptom of chronic stress. Ginsenoside Rd (GRd), the major active compound in Panax ginseng, was previously reported in various neurological researches. However, little research is available regarding on the effect of GRd on cognitive

Ginsenoside Rd attenuates neuroinflammation of dopaminergic cells in culture.

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In Parkinson's disease clinical and experimental evidence suggest that neuroinflammatory changes in cytokines caused by microglial activation contribute to neuronal death. Experimentally, neuroinflammation of dopaminergic neurons can be evoked by lipopolysaccharide (LPS) exposure. In mesencephalic

Antitumor activity of ginsenoside Rd in gastric cancer via up-regulation of Caspase-3 and Caspase-9.

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Ginsenoside Rd (GS-Rd), isolated from the Chinese traditional herbal medicine Panax ginseng, is used for the treatment of cardiovascular diseases, inflammation, different body pains, and trauma. Caspase-3 and Caspase-9 belong to cysteine aspartic acid specific protease (Caspase) family that

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