Quercetin Improves Behavioral Deficiencies, Restores Astrocytes and Microglia, and Reduces Serotonin Metabolism in 3‐Nitropropionic Acid‐Induced Rat Model of Huntington's Disease

CNS Neuroscience and Therapeutics - Tập 20 Số 1 - Trang 10-19 - 2014
Joy Chakraborty1, R. P. Singh1, Debashis Dutta1, Amit K. Naskar1, Usha Rajamma2, Kochupurackal P. Mohanakumar1
1Laboratory of Clinical and Experimental Neuroscience, Division of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
2Manovikas Biomedical Research and Diagnostic Centre, Manovikas Kendra, Kolkata, India

Tóm tắt

SummaryAimHuntington's disease (HD) is an autosomal dominant disorder, for which clinically available drugs offer only symptomatic relief. These prescription drugs are not free of side effects, and the patients usually suffer from anxiety and depression. We investigated quercetin, a dietary flavonoid with free radical scavenging properties, for its beneficial potential if any, in 3‐nitropropionic acid (3‐NP)‐induced HD in rats where both drugs were administered simultaneously.MethodsPerformance of rats on beam balancing, elevated plus maze and gait traits were investigated following 3‐NP and/or quercetin treatments for 4 days. Striatal biogenic amine levels and monoamine oxidase activity were assayed. Striatal sections were examined for Cd11B and glial fibrillary acidic protein immunoreactivity, and for evidences of neuronal lesion.ResultsQuercetin significantly attenuated 3‐NP‐induced anxiety, motor coordination deficits, and gait despair. While the dopaminergic hyper‐metabolism was unaffected, quercetin provided a significant reduction of 3‐NP mediated increase in serotonin metabolism. Quercetin failed to affect 3‐NP‐induced striatal neuronal lesion, but decreased microglial proliferation, and increased astrocyte numbers in the lesion core.ConclusionThese results taken together suggest that quercetin could be of potential use not only for correcting movement disturbances and anxiety in HD, but also for addressing inflammatory damages.

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CNS Neuroscience and Therapeutics

Tập 20 Số 1

10-19

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