Quercetin nanoparticles exhibit a potential therapeutic effect against the neurochemical changes and motor deficits in a rat model of Parkinson's disease.
Quercetin nanoparticles exhibit a potential therapeutic effect against the neurochemical changes and motor deficits in a rat model of Parkinson's disease.
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Original abstract
The present study investigated the therapeutic potential of quercetin nanoparticles (QNPs), administered alone or in combination with levodopa/carbidopa (L/C), against reserpine-induced neurochemical alterations and motor dysfunction in a rat model of Parkinson's disease (PD). Animals were randomly assigned to five experimental groups: a control group, a reserpine-induced PD group, and PD groups treated with QNPs, L/C, or their combination. Motor performance was assessed using the open-field and grid traction tests. Reserpine administration induced marked motor impairments accompanied by significant reductions in dopamine (DA), serotonin (5-HT), and norepinephrine (NE) levels in both the striatum and midbrain. These neurochemical deficits were associated with elevated monoamine oxidase (MAO) activity, increased lipid peroxidation (malondialdehyde, MDA), enhanced acetylcholinesterase (AChE) activity, and increased nitric oxide (NO) levels in both brain regions. Additionally, reduced glutathione (GSH) levels were decreased in the midbrain but elevated in the striatum. Treatment with QNPs significantly restored monoamine levels and normalized MAO and AChE activities. Moreover, QNPs markedly attenuated oxidative stress and improved motor performance in reserpine-treated rats. Similarly, L/C administration effectively reversed monoamine depletion, normalized enzymatic activities, and mitigated oxidative stress. Notably, combined treatment with QNPs and L/C produced effects comparable to those observed with either treatment alone, suggesting a lack of additive or synergistic interaction. These findings demonstrate that QNPs exert a significant neuroprotective effect against reserpine-induced motor dysfunction and neurochemical disturbances, supporting their potential as a therapeutic strategy for Parkinsonian pathology.