Neuron
Article21-Aminosteroids attenuate excitotoxic neuronal injury in cortical cell cultures
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Interweaving epilepsy and neurodegeneration: Vitamin E as a treatment approach
2021, Biomedicine and PharmacotherapyCitation Excerpt :Thus, oxidative stress induce neurodegeneration is a possible mechanism for epileptogenesis, or it may act as contributing factor to seizure-associated neuronal death as it gradually disrupts calcium homeostasis which leads to increased excitability, susceptibility to seizure, and vulnerability to stress and neuronal loss (Fig. 2). The role of ROS in neuronal death due to seizures is supported by shreds of evidence that prolong seizures results in enhanced oxidation of macromolecules and numerous antioxidant compounds found to reverse the excitotoxicity [55–61]. Peroxynitrite, one of the reactive nitrogen species is also produced as a consequence of the reaction between excess ROS and nitric oxide (NO).
Newer pharmacological approaches for antioxidant neuroprotection in traumatic brain injury
2019, NeuropharmacologyCitation Excerpt :Lipid peroxidation-derived neurotoxic aldehydes (carbonyls) 4-HNE or acrolein have been shown in neuronal or astrocytic cultures or in synaptosomes to impair glutamate uptake and to inhibit mitochondrial function (Keller et al., 1997a, 1997b; Lovell et al., 2000; Springer et al., 1997). On the other hands, glutamate and NMDA-induced excitotoxic damage in synaptosomal or neuronal cultures is attenuated by pharmacological LP inhibition confirming that oxidative damage promoters of glutamate excitotoxicity (Monyer et al., 1990) (Pellegrini-Giampietro et al., 1990). The initial studies of free radical scavenging compounds in TBI models were carried out with Cu++/Zn++ SOD in the pioneering work of Kontos and coworkers (Kontos, 1989; Kontos and Povlishock, 1986; Kontos and Wei, 1986).
Pathophysiology
2018, Volpe's Neurology of the NewbornMutations in Plasmalemma Vesicle Associated Protein Result in Sieving Protein-Losing Enteropathy Characterized by Hypoproteinemia, Hypoalbuminemia, and Hypertriglyceridemia
2015, Cellular and Molecular Gastroenterology and HepatologyCitation Excerpt :Because mRNAs with premature stop codons can be targeted for degradation,17,18 we tested whether the mutant PLVAP p.Arg358* mRNA and protein were expressed in patient samples. Quantitative in situ hybridization with PLVAP-specific probes using RNAscope technology11,19 showed a drastic reduction in PLVAP mRNA expression in the patient’s biopsy tissue (see Figure 4A, right panel) whereas the signal was readily detected in biopsies from normal and disease control patients (see Figure 4A left and middle panel). To confirm these findings at the protein level, we first identified an antibody capable of detecting the truncated PLVAP p.Arg358* protein.
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Present address: laboratory of Molecular Neuroendocrinology, ZMBH, University of Heidelberg, INF 282, D-6900 Heidelberg, Federal Republic of Germany.