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Introduction <p>Ro 20–1724, a phosphodiesterase-4 (PDE4) inhibitor, is known to enhance cognition and reduce oxidative stress in the brain. However, its potential effects on Parkinson’s disease (PD) remain unexplored.</p> Aim <p>This study aims to evaluate the neuroprotective effects of Ro 20–1724 in a rotenone-induced PD model using in vitro and in vivo approaches.</p> Methods <p>In vitro, the cytotoxicity of Ro 20–1724 and its protective effects against rotenone-induced toxicity were assessed using the MTT assay in SH-SY5Y human neuroblastoma cells. Apoptotic markers and reactive oxygen species (ROS) production were analyzed using flow cytometry, while pro-inflammatory cytokines were measured using ELISA. In vivo, rats were administered Ro 20–1724 (500&#xa0;µg/kg, i.p.) for 21&#xa0;days in a rotenone-induced PD model. Behavioral assessments, including muscle coordination and locomotor activity, were performed. Oxidative stress markers, endogenous antioxidant enzyme levels, and neuronal integrity were evaluated using biochemical assays and Nissl staining.</p> Results <p>Ro 20–1724 significantly reduced rotenone-induced cytotoxicity in SH-SY5Y cells, decreased ROS levels, and suppressed pro-apoptotic protein expression. It also lowered pro-inflammatory cytokine levels. In vivo, Ro 20–1724 significantly improved muscle coordination and locomotor activity, reduced oxidative stress, and preserved dopaminergic neurons in the substantia nigra. Nissl staining confirmed the protection of neuronal integrity.</p> Conclusion <p>Ro 20–1724 effectively mitigates oxidative stress, apoptosis, and neuroinflammation in a rotenone-induced PD model. It enhances neuronal survival and motor function, suggesting its potential as a promising therapeutic candidate for Parkinson’s disease.</p>

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Modulation of PDE4 activity to counteract neurobehavioral deficits in rotenone-induced parkinsonism

  • 期刊论文

  • 发表日期：

    2026年1月22日

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  • S. K. Meherronnisha,
  • Dithu Thekkekkara,
  • Salini P. Nair,
  • Chaithra S. R.,
  • Karthik G. Pujar,
  • Prabitha P

摘要

Introduction

Ro 20–1724, a phosphodiesterase-4 (PDE4) inhibitor, is known to enhance cognition and reduce oxidative stress in the brain. However, its potential effects on Parkinson’s disease (PD) remain unexplored.

Aim

This study aims to evaluate the neuroprotective effects of Ro 20–1724 in a rotenone-induced PD model using in vitro and in vivo approaches.

Methods

In vitro, the cytotoxicity of Ro 20–1724 and its protective effects against rotenone-induced toxicity were assessed using the MTT assay in SH-SY5Y human neuroblastoma cells. Apoptotic markers and reactive oxygen species (ROS) production were analyzed using flow cytometry, while pro-inflammatory cytokines were measured using ELISA. In vivo, rats were administered Ro 20–1724 (500 µg/kg, i.p.) for 21 days in a rotenone-induced PD model. Behavioral assessments, including muscle coordination and locomotor activity, were performed. Oxidative stress markers, endogenous antioxidant enzyme levels, and neuronal integrity were evaluated using biochemical assays and Nissl staining.

Results

Ro 20–1724 significantly reduced rotenone-induced cytotoxicity in SH-SY5Y cells, decreased ROS levels, and suppressed pro-apoptotic protein expression. It also lowered pro-inflammatory cytokine levels. In vivo, Ro 20–1724 significantly improved muscle coordination and locomotor activity, reduced oxidative stress, and preserved dopaminergic neurons in the substantia nigra. Nissl staining confirmed the protection of neuronal integrity.

Conclusion

Ro 20–1724 effectively mitigates oxidative stress, apoptosis, and neuroinflammation in a rotenone-induced PD model. It enhances neuronal survival and motor function, suggesting its potential as a promising therapeutic candidate for Parkinson’s disease.