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Ginsenoside rd in experimental stroke: superior neuroprotective efficacy with a wide therapeutic window.

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Ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, has been demonstrated to protect against ischemic cerebral damage in vitro and in vivo. In this study, we aimed to further define the preclinical characteristics of Rd. We show that Rd passes the intact blood-brain barrier and

Ginsenoside Rd attenuates redox imbalance and improves stroke outcome after focal cerebral ischemia in aged mice.

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We previously found that ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, protects against ischemic brain damage induced by oxygen-glucose deprivation in vitro and middle cerebral artery occlusion (MCAO) in vivo. Considering stroke happens frequently in aged individuals, we

Ginsenoside-Rd, a new voltage-independent Ca2+ entry blocker, reverses basilar hypertrophic remodeling in stroke-prone renovascular hypertensive rats.

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The total saponins of Panax notoginseng have been clinically used for the treatment of cardiovascular diseases and stroke in China. Our recent study has identified ginsenoside-Rd, a purified component of total saponins of P. notoginseng, as an inhibitor to remarkably inhibit voltage-independent

Ginsenoside-Rd improves outcome of acute ischaemic stroke - a randomized, double-blind, placebo-controlled, multicenter trial.

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OBJECTIVE Ginsenoside-Rd is a receptor-operated calcium channel antagonist and has shown promise as a neuroprotectant in our phase II study. As an extended work, we sought to confirm its efficacy and safety of Ginsenoside-Rd in patients with acute ischaemic stroke. METHODS We conducted a randomized,

Ginsenoside Rd for acute ischemic stroke: translating from bench to bedside.

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Numerous studies have identified pathophysiological mechanisms of acute ischemic stroke and have provided proof-of-principle evidence that strategies designed to impede the ischemic cascade, namely neuroprotection, can protect the ischemic brain. However, the translation of these therapeutic agents

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 and ischemic stroke; a short review of literatures.

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Panax ginseng is a well-known economic medical plant that is widely used in Chinese traditional medicine. This species contains a unique class of natural products-ginsenosides. Recent clinical and experimental studies have presented numerous lines of evidence on the promising role of ginsenosides on

Efficacy and safety of ginsenoside-Rd for acute ischaemic stroke: a randomized, double-blind, placebo-controlled, phase II multicenter trial.

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OBJECTIVE Ginsenoside-Rd is a selective competitive Ca2+ receptor antagonist. A phase II randomized, double-blind, placebo-controlled, multicenter study was conducted to examine the efficacy and safety of ginsenoside-Rd in patients with acute ischaemic stroke. METHODS A total of 199 patients were

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

Pharmacokinetics and safety of ginsenoside Rd following a single or multiple intravenous dose in healthy Chinese volunteers.

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The pharmacokinetics and safety of ginsenoside Rd (Rd) were assessed in healthy Chinese volunteers. In the single-dose study, a randomized, open-label, 3-way crossover design was used. Participants were assigned to receive 10, 45, or 75 mg Rd by intravenous infusion, with a 2-week washout period

Ginsenoside Rd protects neurons against glutamate-induced excitotoxicity by inhibiting ca(2+) influx.

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Our previous studies have demonstrated that ginsenoside Rd (GSRd), one of the principal ingredients of Pana notoginseng, has neuroprotective effects against ischemic stroke. However, the possible mechanism(s) underlying the neuroprotection of GSRd is/are still largely unknown. In this study, we

Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons.

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We previously found that ginsenoside Rd (GSRd), one of the main active ingredients in Panax Ginseng, attenuates H(2)O(2)-induced oxidative injury in PC12 cells. Mounting evidence suggests that the oxidative stress is crucially involved in the pathophysiologic process of ischemia. In the present

Ginsenoside Rd Attenuates DNA Damage by Increasing Expression of DNA Glycosylase Endonuclease VIII-like Proteins after Focal Cerebral Ischemia.

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BACKGROUND Ginsenoside Rd (GSRd), one of the main active ingredients in traditional Chinese herbal Panax ginseng, has been found to have therapeutic effects on ischemic stroke. However, the molecular mechanisms of GSRd's neuroprotective function remain unclear. Ischemic stroke-induced oxidative

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 inhibits apoptosis following spinal cord ischemia/reperfusion injury.

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Ginsenoside Rd has a clear neuroprotective effect against ischemic stroke. We aimed to verify the neuroprotective effect of ginsenoside Rd in spinal cord ischemia/reperfusion injury and explore its anti-apoptotic mechanisms. We established a spinal cord ischemia/reperfusion injury model in rats

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