It is well known that an excessive release of glutamate in the mammalian brain plays a major role in several neurological diseases. Naftazone (Etioven®) is a currently used vasoprotectant drug that is metabolized in humans by reduction and glucuronidation. In the present study naftazone was found to decrease glutamate levels in the cerebro spinal fluid (CSF) of rats treated for 15 days, as determined by a chemiluminescent glutamate assay reaction. Naftazone and its glucuronide derivative also reduced respectively spontaneous and high K+-evoked glutamate release from mouse cerebellum synaptosomes. It is likely that naftazone and its glucuronide metabolite contribute in vivo to decrease glutamate levels in the CSF through their inhibitory actions on glutamate release.
peekaboo wrote:I wonder if there is a supplement out there that doesn't include pharma!
Abstract (-)-Epigallocatechin-3-gallate (EGCG) is a major polyphenol in green tea. Many health promoting effects of EGCG have been reported based on its antioxidative and gene modulation properties, but no study has demonstrated a protective effect of EGCG against glutamate-induced neuronal damage. Excessive glutamate stimulation on neuronal cells leads to accumulation of reactive oxygen species (ROS) which ultimately contribute to cell death in stroke, trauma and other neurodegenerative disorders. In this study, mouse hippocampal cell line, HT-22, was used to determine the effect of EGCG on glutamate neurotoxicity. It was found that EGCG protected HT-22 cells against glutamate neurotoxicity when administered 10 h after glutamate incubation. The protective action of EGCG is mainly due to its antioxidative effect.
dignan wrote:Cheer, naftazone sounds interesting. I wonder if anybody is thinking of testing it for MS patients.
estrogens protect cultured hippocampal neurons against glutamate toxicity, glucose deprivation, FeSO4 toxicity, and amyloid beta-peptide (A beta) toxicity.
The toxicity of each insult was significantly attenuated in cultures pretreated for 2 h with 100 nM-10 microM 17 beta-estradiol, estriol, or progesterone.
In contrast, corticosterone exacerbated neuronal injury induced by glutamate
we demonstrate that minocycline-induced neuroprotection is related to a direct antagonism of multiple mechanisms leading to neuronal cell death such as the induction of anti-apoptotic intracellular signalling pathways and a decrease in glutamate excitotoxicity.
From these observations, we conclude that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties.
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