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<p>Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and oxidative stress–induced apoptosis. The present study evaluated the neuroprotective potential of cirsimaritin against MPTP-induced PD in mice and explored its possible mechanism through combined in silico and in vivo approaches. Molecular docking using AutoDock Vina revealed that cirsimaritin exhibits strong binding affinities with key antioxidant enzymes (CAT, GPx, and SOD) and apoptosis-related proteins (Bcl-2, Bax, caspase-3, −8, and − 9), suggesting possible modulation of oxidative and apoptotic signaling pathways. In vivo, PD was induced by MPTP (30&#xa0;mg/kg, i.p., for 7&#xa0;days), followed by oral administration of cirsimaritin (25 and 50&#xa0;mg/kg). Behavioral assessments—including the open field, narrow beam walking, and wire hanging tests—demonstrated significant improvement in locomotor and neuromuscular performance in cirsimaritin-treated mice. Biochemical analyses revealed that cirsimaritin restored dopamine and its metabolites, decreased lipid peroxidation (TBARS), and enhanced antioxidant enzyme activities (CAT, SOD, and GPx). Additionally, cirsimaritin attenuated apoptosis by upregulating Bcl-2 and downregulating Bax and caspase-3 expression. Histopathological examination confirmed reduced neurodegeneration in the brain hippocampus of treated mice. These findings indicate that cirsimaritin exerts potent neuroprotective effects in MPTP-induced PD mice, likely through its antioxidant and anti-apoptotic actions, supporting its potential as a therapeutic candidate for Parkinson’s disease.</p>

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Evaluation of the Neuroprotective Efficacies and Related Mechanisms of Cirsimaritin in MPTP-Induced Parkinson in Mice with Following the Molecular Docking Studies

  • 期刊论文

  • 发表日期：

    2026年3月4日

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  • Yan Wei,
  • Qi Li,
  • Abdurahman Hajinur Hirad,
  • Abdullah A. Alarfaj,
  • Indumathi Thangavelu,
  • Palanisamy Arulselvan

摘要

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and oxidative stress–induced apoptosis. The present study evaluated the neuroprotective potential of cirsimaritin against MPTP-induced PD in mice and explored its possible mechanism through combined in silico and in vivo approaches. Molecular docking using AutoDock Vina revealed that cirsimaritin exhibits strong binding affinities with key antioxidant enzymes (CAT, GPx, and SOD) and apoptosis-related proteins (Bcl-2, Bax, caspase-3, −8, and − 9), suggesting possible modulation of oxidative and apoptotic signaling pathways. In vivo, PD was induced by MPTP (30 mg/kg, i.p., for 7 days), followed by oral administration of cirsimaritin (25 and 50 mg/kg). Behavioral assessments—including the open field, narrow beam walking, and wire hanging tests—demonstrated significant improvement in locomotor and neuromuscular performance in cirsimaritin-treated mice. Biochemical analyses revealed that cirsimaritin restored dopamine and its metabolites, decreased lipid peroxidation (TBARS), and enhanced antioxidant enzyme activities (CAT, SOD, and GPx). Additionally, cirsimaritin attenuated apoptosis by upregulating Bcl-2 and downregulating Bax and caspase-3 expression. Histopathological examination confirmed reduced neurodegeneration in the brain hippocampus of treated mice. These findings indicate that cirsimaritin exerts potent neuroprotective effects in MPTP-induced PD mice, likely through its antioxidant and anti-apoptotic actions, supporting its potential as a therapeutic candidate for Parkinson’s disease.