Moreno-Ortega 2016 Neurotox Res: Difference between revisions
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{{Publication | {{Publication | ||
|title=Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Ríos C, García AG, Ruiz-Nuño A, Cano-Abad MF (2016) Neuroprotective effect of the novel compound ITH33/IQM9.21 against oxidative stress and Na< | |title=Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Ríos C, García AG, Ruiz-Nuño A, Cano-Abad MF (2016) Neuroprotective effect of the novel compound ITH33/IQM9.21 against oxidative stress and Na<sup>+</sup> and Ca<sup>2+</sup> overload in motor neuron-like NSC-34 cells. Neurotox Res 30:380-91. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/27126806 PMID: 27126806] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/27126806 PMID: 27126806] | ||
|authors=Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Rios C, Garcia AG, Ruiz-Nuno A, Cano-Abad MF | |authors=Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Rios C, Garcia AG, Ruiz-Nuno A, Cano-Abad MF | ||
|year=2016 | |year=2016 | ||
|journal=Neurotox Res | |journal=Neurotox Res | ||
|abstract=Alternatives for the treatment of amyotrophic lateral sclerosis (ALS) are scarce and controversial. The etiology of neuronal vulnerability in ALS is being studied in motor neuron-like NSC-34 cells to determine the underlying mechanisms leading to selective loss of motor neurons. One such mechanism is associated with mitochondrial oxidative stress, Ca< | |abstract=Alternatives for the treatment of amyotrophic lateral sclerosis (ALS) are scarce and controversial. The etiology of neuronal vulnerability in ALS is being studied in motor neuron-like NSC-34 cells to determine the underlying mechanisms leading to selective loss of motor neurons. One such mechanism is associated with mitochondrial oxidative stress, Ca<sup>2+</sup> overload, and low expression of Ca<sup>2+</sup>-buffering proteins. Therefore, in order to elicit neuronal death in ALS, NSC-34 cells were exposed to the following cytotoxic agents: (1) a mixture of oligomycin 10 µM and rotenone 30 µM (O/R), or (2) phenylarsine oxide 1 µM (PAO) (to mimic excess free radical production during mitochondrial dysfunction), and (3) veratridine 100 µM (VTD) (to induce overload of Na(+) and Ca<sup>2+</sup> and to alter distribution of Ca<sup>2+</sup>-buffering proteins [parvalbumin and calbindin-D28k]). Thus, the aim of the study was to test the novel neuroprotective compound ITH33/IQM9.21 (ITH33) and to compare it with riluzole on ''in vitro'' models of neurotoxicity. Cell viability measured with MTT showed that only ITH33 protected against O/R at 3 μM and PAO at 10 μM, but not riluzole. ITH33 and riluzole were neuroprotective against VTD, blocked the maximum peak and the number of [Ca<sup>2+</sup>]c oscillations per cell, and restored the effect on parvalbumin. However, only riluzole reversed the effect on calbindin-D28k levels. Therefore, ITH33 was neuroprotective against oxidative stress and Na<sup>+</sup>/Ca<sup>2+</sup> overload, both of which are involved in ALS. | ||
|keywords=Amyotrophic lateral sclerosis, Ca< | |keywords=Amyotrophic lateral sclerosis, Ca<sup>2+</sup>, ITH33/IQ9.21, Mitochondria, NSC-34 cells, Veratridine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Latest revision as of 13:42, 10 October 2016
| Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Ríos C, García AG, Ruiz-Nuño A, Cano-Abad MF (2016) Neuroprotective effect of the novel compound ITH33/IQM9.21 against oxidative stress and Na+ and Ca2+ overload in motor neuron-like NSC-34 cells. Neurotox Res 30:380-91. |
Moreno-Ortega AJ, Al-Achbili LM, Alonso E, de Los Rios C, Garcia AG, Ruiz-Nuno A, Cano-Abad MF (2016) Neurotox Res
Abstract: Alternatives for the treatment of amyotrophic lateral sclerosis (ALS) are scarce and controversial. The etiology of neuronal vulnerability in ALS is being studied in motor neuron-like NSC-34 cells to determine the underlying mechanisms leading to selective loss of motor neurons. One such mechanism is associated with mitochondrial oxidative stress, Ca2+ overload, and low expression of Ca2+-buffering proteins. Therefore, in order to elicit neuronal death in ALS, NSC-34 cells were exposed to the following cytotoxic agents: (1) a mixture of oligomycin 10 µM and rotenone 30 µM (O/R), or (2) phenylarsine oxide 1 µM (PAO) (to mimic excess free radical production during mitochondrial dysfunction), and (3) veratridine 100 µM (VTD) (to induce overload of Na(+) and Ca2+ and to alter distribution of Ca2+-buffering proteins [parvalbumin and calbindin-D28k]). Thus, the aim of the study was to test the novel neuroprotective compound ITH33/IQM9.21 (ITH33) and to compare it with riluzole on in vitro models of neurotoxicity. Cell viability measured with MTT showed that only ITH33 protected against O/R at 3 μM and PAO at 10 μM, but not riluzole. ITH33 and riluzole were neuroprotective against VTD, blocked the maximum peak and the number of [Ca2+]c oscillations per cell, and restored the effect on parvalbumin. However, only riluzole reversed the effect on calbindin-D28k levels. Therefore, ITH33 was neuroprotective against oxidative stress and Na+/Ca2+ overload, both of which are involved in ALS. • Keywords: Amyotrophic lateral sclerosis, Ca2+, ITH33/IQ9.21, Mitochondria, NSC-34 cells, Veratridine
Labels: MiParea: Pharmacology;toxicology
Pathology: Cardiovascular
Organism: Mouse Tissue;cell: Nervous system
