Effects of gold nanoparticles administration through behavioral and oxidative parameters in animal model of Parkinson’s disease

• Published in: Colloids and surfaces, B, Biointerfaces B, Biointerfaces, 2020-12, Vol.196, p.111302, Article 111302
• Main Authors: da Silva Córneo, Emily, de Bem Silveira, Gustavo, Scussel, Rahisa, Correa, Maria Eduarda Anastácio Borges, da Silva Abel, Jessica, Luiz, Gabriel Paulino, Feuser, Paulo Emilio, Silveira, Paulo Cesar Lock, Machado-de-Ávila, Ricardo Andrez
• Format: Article
• Language: English
• Subjects: Behavioral; Gold nanoparticles; Neurotrophins; Oxidative stress; Parkinson’s disease
• ISSN: 0927-7765; 1873-4367
• DOI: 10.1016/j.colsurfb.2020.111302

[Display omitted] •Symptoms in animals proved to be similar to the behavioral characteristics of individuals with PD.•GNP treatment reversed behavioral symptoms caused by reserpine.•GNPs reversed the symptoms of PD caused by reserpine in C57BL/6 mice, especially without toxicity.•GNPs shows promise and showed antioxidant and neuroprotective effects. Parkinson's disease (PD) is recognized as the second most common neurodegenerative disorder, after Alzheimer’s disease. Reserpine administration to animals has been suggested as a PD model based on the effects of this monoamine-depleting agent on motor activity. Studies show that gold nanoparticles (GNPs) are effective for treating neurodegenerative diseases when used at certain concentrations. The objective of the present study was to evaluate the effects of GNPs administration under behavioral and oxidative stress conditions in an experimental model of PD. Fourty male C57BL/6 mice (20–30 g) were used, The animals were divided into four groups (N = 6): Sham; Sham and GNPs; Reserpine; Reserpine and GNPs. Three doses at the concentration of 0.25 mg/kg reserpine were administered subcutaneously at 48 h intervals. Treatment with GNPs was administered with 2.5 mg/kg GNPs (20 nm) for five consecutive days. Our results showed the therapeutic potential of GNPs, where the parameters observed in behavioral tests and oxidative stress were reverted in GNP-treated mice. It also partially improved neurotrophic factors, which are necessary for the survival of neurons. GNPs reversed the symptoms of PD caused by the use of alkaline reserpine in C57BL/6 mice, especially without toxicity. The results of this study suggest that GNPs could have clinical potential as an inhibitor of inflammation and oxidative stress in the CNS, thereby alleviating the secondary neurodegenerative processes and neuronal cell death caused by reserpine. These beneficial effects of GNPs provide support for new analyses to better understanding in the process of PD degeneration.