Therapeutic Effects of Citral Nanoliposome on Parkinson’s Treatment in a Rat Model: Modulation via Neurochemical, Inflammatory and Antioxidant Pathways

Abstract

Parkinson’s disease is the most common neurodegenerative movement disorder, the pathogenesis of which is partly related with oxidant status and inflammatory responses. The administration of citral with antioxidant and anti-inflammatory properties may alleviate the negative effects of Parkinson. The present study aimed to assess the effects of citral nanoliposome on Parkinson’s treatment in a rat model. In this study, citral nanoliposome was successfully produced through employing a facile method. Additionally, 40 Wistar rats were divided into four groups (n = 10), one of which was considered as Sham and received no treatment. However, the other groups were administrated with rotenone, and/or treated with 5 and 10 mg/kg of citral for 21 days. Behavioral responses were evaluated based on the forced swimming test and hippocampal-dependent memory deficit. The rates were examined for tissue lipid peroxide (LPO), as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in brain. Further, they were investigated in terms of expression of brain-derived neurotrophic factor (BDNF), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), and nuclear factor kappa B (NF-κB). The results suggested more immobility, higher LPO level, and a rise in the expression of TNF-α, IL-6, and NF-κB (P = 0.001) following rotenone administration. Furthermore, this treatment decreased climbing, retention latency, SOD and GPx activities, and BDNF expression (P = 0.001). The use of citral, especially in higher dose, reversed all the adverse effects of rotenone on behavioral responses, antioxidant status, BDNF, and inflammatory genes. Parkinson represents a closed relationship with movement deficiency, increased inflammation, and reduced oxidant status. Citral administration can be considered as a therapeutic option following future studies.