Neuroprotective effects of 2-(2-nitrophenyl)-1,3-thiazolidine-4-carboxylic acid in a rotenone-induced Parkinson's disease rat model: Modulation of oxidative stress, behavioral dysfunction, and iron accumulation.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss, oxidative stress, and abnormal iron accumulation in the substantia nigra. Targeting redox imbalance and metal dysregulation represents a promising therapeutic strategy. This study evaluated the neuroprotective potential of 2-(2-nitrophenyl)-1,3-thiazolidine-4-carboxylic acid (2,2Np-1,3TZD-4-CA) in a rotenone-induced rat model of PD. Forty-two male Sprague-Dawley rats were randomly assigned to seven experimental groups, including controls, rotenone-treated animals, compound-treated groups, and combined treatment groups. Behavioral performance was assessed using pole, inverted screen, rotarod, Y-maze, open field, and tail suspension tests. Oxidative stress markers (SOD, CAT, MDA, GSH, GPx) were measured, along with brain iron analysis and histopathological examination. Treatment with 2,2Np-1,3TZD-4-CA significantly improved rotenone-induced behavioral impairments and restored antioxidant enzyme activities (P < 0.05). Moreover, the compound reduced elevated brain iron levels and ameliorated histopathological alterations in neural tissues (P < 0.05), indicating attenuation of oxidative and metabolic damage. These findings demonstrate that 2,2Np-1,3TZD-4-CA exerts marked neuroprotective effects, likely mediated through regulation of oxidative stress and iron homeostasis, suggesting its potential therapeutic relevance for Parkinson's disease.