Quinolinic Acid-Induced Huntington Disease-Like Symptoms Mitigated by Potent Free Radical Scavenger Edaravone—a Pilot Study on Neurobehavioral, Biochemical, and Histological Approach in Male Wistar Rats

Abstract

In this study, we demonstrated for the first time the neuroprotective role of edaravone (Eda) (5 and 10mg/kg b.w.), a potent free radical scavenger against the unilateral stereotaxic induction of quinolinic acid (QA) (300nm/4μl saline)-induced Huntington disease (HD)-like symptoms in behavioral, biochemical, and histological features in male Wistar rats striatum. QA induction, which mimics the early stage of HD, commonly causes oxidative stress to the cell and decreases the antioxidant defense mechanism by altering the level of lipid peroxidation (LPO), protein carbonyls, and nitrate concentration (NO) and the activities of glutathione family enzymes (GPx, GST, GR) and acetyl choline esterase concentration (AChE) which was found to be ameliorated by Eda treatment in both the tested doses 5 and 10mg/kg b.w. in the significance of P <0.05 and P <0.01, respectively. Finally histopathological analysis by hematoxylin and eosin stain concluded the promising neurodefensive role of Eda in rat striatum at the dosage of 10mg/kg b.w., with the decreased tissue damage and the number of damaged granular cells when compared to QA-induced groups.