Edaravone alleviates cisplatin-induced neurobehavioral deficits via modulation of oxidative stress and inflammatory mediators in the rat hippocampus.

doi:10.1016/j.ejphar.2016.08.003

Paper

Edaravone alleviates cisplatin-induced neurobehavioral deficits via modulation of oxidative stress and inflammatory mediators in the rat hippocampus.

Published Nov 15, 2016 · A. Jangra, M. Kwatra, Tavleen Singh

European journal of pharmacology

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74

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Abstract

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Animal Study

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Study Snapshot

Edaravone treatment prevents neurobehavioral deficits caused by cisplatin by modulating oxidative stress and inflammatory mediators in the rat hippocampus.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Edaravone alleviates cisplatin-induced neurobehavioral deficits via modulation of oxidative stress and inflammatory mediators in the rat hippocampus.

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References

Naringin and Sertraline Ameliorate Doxorubicin-Induced Behavioral Deficits Through Modulation of Serotonin Level and Mitochondrial Complexes Protection Pathway in Rat Hippocampus

Naringin and sertraline treatment, alone or combined, can improve behavioral deficits and reduce neuroinflammation caused by doxorubicin in rats.

Lipopolysaccharide-Induced Behavioral Alterations Are Alleviated by Sodium Phenylbutyrate via Attenuation of Oxidative Stress and Neuroinflammatory Cascade

Sodium phenylbutyrate (SPB) shows neuroprotective potential in reducing anxiety and depressive-like behavior in mice by reducing oxidative stress and neuroinflammation.

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Naringin can be used in combination with doxorubicin due to its high cardioprotective effect against doxorubicin-induced cardiomyopathy in rats.

Increased oxidative stress in patients with amyotrophic lateral sclerosis and the effect of edaravone administration

Edaravone administration effectively reduces oxidative stress in ALS patients, potentially enhancing their functional recovery.

Sodium Phenylbutyrate and Edaravone Abrogate Chronic Restraint Stress-Induced Behavioral Deficits: Implication of Oxido-Nitrosative, Endoplasmic Reticulum Stress Cascade, and Neuroinflammation

Sodium phenylbutyrate and edaravone effectively improve cognitive deficits and anxiety- and depressive-like behavior in mice, potentially due to inhibition of oxido-nitrosative stress, neuroinflammation, and ER stress cascade.

Edaravone abrogates LPS-induced behavioral anomalies, neuroinflammation and PARP-1

Edaravone pretreatment prevents LPS-induced anxiety and depressive-like behavior by reducing inflammation, oxido-nitrosative stress, and PARP-1 overexpression in the hippocampus.

Lipopolysaccharide induced anxiety- and depressive-like behaviour in mice are prevented by chronic pre-treatment of esculetin

Esculetin prevents LPS-induced anxiety and depressive-like behavior in mice, potentially due to inhibition of cytokine production, oxidative stress, and plasma CORT levels.

Honokiol abrogates chronic restraint stress-induced cognitive impairment and depressive-like behaviour by blocking endoplasmic reticulum stress in the hippocampus of mice.

Honokiol reduces cognitive impairment and depressive-like behavior in mice by blocking endoplasmic reticulum stress in the hippocampus.

t-BHQ Provides Protection against Lead Neurotoxicity via Nrf2/HO-1 Pathway

T-BHQ protects against lead neurotoxicity by reducing oxidative stress and promoting neuronal survival through the Nrf2/HO-1 pathway.

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