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Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling.

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OBJECTIVE Ginsenoside Rb1 (Rb1) has been reported to have varieties of neuroprotective effects. This study aimed to evaluate the effects of Rb1 on pentylenetetrazol (PTZ)-induced rat brain injury and Mg2+ free-induced neuron injury and analyzed the detailed molecular mechanisms in vivo and in

Anticonvulsant activity of ginseng on seizures induced by chemical convulsants.

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OBJECTIVE To test the anticonvulsant activity of three preparations of American ginseng: whole root extract, whole leaves/stems extract, and a partially purified extract that concentrates the Rb ginsenosides (Rb extract). METHODS One hour after treatment with normal saline, or one of the three

The Effects of Ginsenoside Compound K Against Epilepsy by Enhancing the γ-Aminobutyric Acid Signaling Pathway.

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The imbalance between the GABA-mediated inhibition and the glutamate-mediated excitation is the primary pathological mechanism of epilepsy. GABAergic and glutamatergic neurotransmission have become the most important targets for controlling epilepsy. Ginsenoside compound K (GCK) is a main metabolic

Anticonvulsant and neuroprotective effects of ginsenosides in rats.

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A partially purified extract from American ginseng has been shown to have anticonvulsant activity. To identify the active components in this extract, the activities of the individual ginsenosides (Rb(1), Rb(3) and Rd), mixtures of the purified ginsenosides and a newly prepared Rb fraction were

Passiflora caerulea L. fruit extract and its metabolites ameliorate epileptic seizure, cognitive deficit and oxidative stress in pilocarpine-induced epileptic mice.

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The anticonvulsant potential of aqueous fruit extract of Passiflora caerulea (PCAE) was evaluated in swiss albino mice induced by pilocarpine. The antioxidant activities of PCAE were determined which showed strong antioxidant activity and the polyphenol compounds such as ginsenoside, naringenin,

Ginsenosides inhibit NMDA receptor-mediated epileptic discharges in cultured hippocampal neurons.

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Epilepsy or the occurrence of spontaneous recurrent epileptiform discharges (SREDs, seizures) is one of the most common neurological disorders. Shift in the balance of brain between excitatory and inhibitory functions due to different types of structural or functional alterations may cause

Ginsenosides attenuate kainic acid-induced synaptosomal oxidative stress via stimulation of adenosine A(2A) receptors in rat hippocampus.

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Treatment with ginsenosides attenuated KA-induced seizures and oxidative stress in the synaptosome, and reduced synaptic vesicles at the presynaptic terminals dose-dependently. The adenosine A(2A) receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl) xanthine reversed the ginsenoside-mediated

Ginsenoside Rd as a potential neuroprotective agent prevents trimethyltin injury.

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Trimethyltin (TMT) is a potent neurotoxicant that affects various regions within the central nervous system, including the neocortex, cerebellum, and hippocampus. In the present study, ginsenoside Rd was investigated as a candidate neuroprotective agent in a primary hippocampal neuron culture and

Ginsenoside Rg3 and Rh2 protect trimethyltin-induced neurotoxicity via prevention on neuronal apoptosis and neuroinflammation.

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The acute exposure of trimethyltin (TMT) develops clinical syndrome characterized by amnesia, aggressive behavior, and complex seizures. This neurotoxicant selectively induces hippocampal neuronal injury and glial activation accompanied with resultant neuroinflammation. Here we report two candidates

Natural or plant products for the treatment of neurological disorders: current knowledge.

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BACKGROUND In recent decades, complementary and alternative medicine (CAM) has become very popular in the treatment of several chronic diseases. Natural products as one of the CAM modalities offer potential opportunities to discover lead compounds for novel drug development. The use of CAM or

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