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Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons

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ABSTRACT

Glutamate is an important excitatory neurotransmitter in mammalian brains, but excessive amount of glutamate can cause “excitotoxicity” and lead to neuronal death. As bipolar neurons, spiral ganglion neurons (SGNs) function as a “bridge” in transmitting auditory information from the ear to the brain and can be damaged by excessive glutamate which results in sensorineural hearing loss. In this study, edaravone, a free radical scavenger, elicited both preventative and therapeutic effects on SGNs against glutamate-induced cell damage that was tested by MTT assay and trypan blue staining. Ho.33342 and PI double staining revealed that apoptosis as well as necrosis took place during glutamate treatment, and apoptosis was the main type of cell death. Oxidative stress played an important role in glutamate-induced cell damage but pretreatment with edaravone alleviated cell death. Results of western blot demonstrated that mechanisms underlying the toxicity of glutamate and the protection of edaravone were related to the PI3K pathway and Bcl-2 protein family.

No MeSH data available.


Related in: MedlinePlus

Changes of SOD activity, MDA level, and GSH content in different groups. Compared with the control group, glutamate decreased activity of SOD, content of SOD, and elevated level of MDA markedly. Edaravone protected SGNs by reversing these changes. ∗p < 0.05. The data shown here was the mean ± SEM of three separate experiments.
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fig7: Changes of SOD activity, MDA level, and GSH content in different groups. Compared with the control group, glutamate decreased activity of SOD, content of SOD, and elevated level of MDA markedly. Edaravone protected SGNs by reversing these changes. ∗p < 0.05. The data shown here was the mean ± SEM of three separate experiments.

Mentions: By taking control as 100%, treatment of SGNs with 2 mM glutamate decreases activity of SOD to 35% and level of GSH to 30% and increased content of MDA to 190%. Pretreatment of edaravone (500 μM) reversed these changes to approximately normal levels, with activity of SOD to 90%, level of GSH to 115%, and content of MDA to 105% (Figure 7). These changes were all statistically significant (∗p < 0.05).


Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons
Changes of SOD activity, MDA level, and GSH content in different groups. Compared with the control group, glutamate decreased activity of SOD, content of SOD, and elevated level of MDA markedly. Edaravone protected SGNs by reversing these changes. ∗p < 0.05. The data shown here was the mean ± SEM of three separate experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5121579&req=5

fig7: Changes of SOD activity, MDA level, and GSH content in different groups. Compared with the control group, glutamate decreased activity of SOD, content of SOD, and elevated level of MDA markedly. Edaravone protected SGNs by reversing these changes. ∗p < 0.05. The data shown here was the mean ± SEM of three separate experiments.
Mentions: By taking control as 100%, treatment of SGNs with 2 mM glutamate decreases activity of SOD to 35% and level of GSH to 30% and increased content of MDA to 190%. Pretreatment of edaravone (500 μM) reversed these changes to approximately normal levels, with activity of SOD to 90%, level of GSH to 115%, and content of MDA to 105% (Figure 7). These changes were all statistically significant (∗p < 0.05).

View Article: PubMed Central - PubMed

ABSTRACT

Glutamate is an important excitatory neurotransmitter in mammalian brains, but excessive amount of glutamate can cause &ldquo;excitotoxicity&rdquo; and lead to neuronal death. As bipolar neurons, spiral ganglion neurons (SGNs) function as a &ldquo;bridge&rdquo; in transmitting auditory information from the ear to the brain and can be damaged by excessive glutamate which results in sensorineural hearing loss. In this study, edaravone, a free radical scavenger, elicited both preventative and therapeutic effects on SGNs against glutamate-induced cell damage that was tested by MTT assay and trypan blue staining. Ho.33342 and PI double staining revealed that apoptosis as well as necrosis took place during glutamate treatment, and apoptosis was the main type of cell death. Oxidative stress played an important role in glutamate-induced cell damage but pretreatment with edaravone alleviated cell death. Results of western blot demonstrated that mechanisms underlying the toxicity of glutamate and the protection of edaravone were related to the PI3K pathway and Bcl-2 protein family.

No MeSH data available.


Related in: MedlinePlus