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<p>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 (<i>P</i> &lt; 0.05). Moreover, the compound reduced elevated brain iron levels and ameliorated histopathological alterations in neural tissues (<i>P</i> &lt; 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.</p> Graphical abstract <p>The figure was generated with Biorender.com (Agreement number: BZ29F2HBKN; Dated: 28-February-2026).</p> <p></p>

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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

  • 期刊论文

  • 发表日期：

    2026年7月1日

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  • Shaheen Kousar,
  • Shazia Perveen,
  • Imran Haider,
  • Sumaira Kanwal,
  • Sana Javaid,
  • Ahmed O. Abbas,
  • Hesham Hassanien,
  • Abdallah Tageldein Mansour,
  • Mohamed Ashour,
  • Mohamed Shawky

摘要

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.

Graphical abstract

The figure was generated with Biorender.com (Agreement number: BZ29F2HBKN; Dated: 28-February-2026).