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<p>Parkinson’s disease, a neurodegenerative disorder, is characterized by the degeneration of dopaminergic neurons and the accumulation of α-synuclein, both of which are aggravated by oxidative stress. This study utilized rotenone-treated SH-SY5Y cells to assess cell viability, ROS levels, and mitochondrial function. RNA-seq, mass spectrometry, and Co-IP analyses identified BDNF-regulated proteins linked to oxidative stress. In rotenone-induced PD mice, evaluations were made of motor performance, neuronal degeneration, and protein expression. Results showed that a 36-h exposure to 0.5&#xa0;µM rotenone significantly increased ROS production, impaired mitochondrial function, and caused cellular damage in SH-SY5Y cells, effects which were reversed by BDNF overexpression. In mice, BDNF overexpression in the substantia nigra pars compacta alleviated PD-like symptoms. Co-IP analysis showed that BDNF modulates NRF2 and its associated proteins via HSP90AA1. These findings demonstrate that BDNF alleviates rotenone-induced oxidative stress in PD models through the HSP90AA1/NRF2 pathway, offering critical insights into the pathogenesis and potential therapeutic strategies for Parkinson’s disease.</p>

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Regulation of HSP90AA1/NRF2 by BDNF Contributes to the Attenuation of Rotenone-Induced Oxidative Stress in Parkinson’s Disease Models

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Song Xie,
  • Wanwan Cao,
  • Jun Guo,
  • Mengfan Zhao,
  • Linxi Wang,
  • Feiteng Liang,
  • Zhao Wang

摘要

Parkinson’s disease, a neurodegenerative disorder, is characterized by the degeneration of dopaminergic neurons and the accumulation of α-synuclein, both of which are aggravated by oxidative stress. This study utilized rotenone-treated SH-SY5Y cells to assess cell viability, ROS levels, and mitochondrial function. RNA-seq, mass spectrometry, and Co-IP analyses identified BDNF-regulated proteins linked to oxidative stress. In rotenone-induced PD mice, evaluations were made of motor performance, neuronal degeneration, and protein expression. Results showed that a 36-h exposure to 0.5 µM rotenone significantly increased ROS production, impaired mitochondrial function, and caused cellular damage in SH-SY5Y cells, effects which were reversed by BDNF overexpression. In mice, BDNF overexpression in the substantia nigra pars compacta alleviated PD-like symptoms. Co-IP analysis showed that BDNF modulates NRF2 and its associated proteins via HSP90AA1. These findings demonstrate that BDNF alleviates rotenone-induced oxidative stress in PD models through the HSP90AA1/NRF2 pathway, offering critical insights into the pathogenesis and potential therapeutic strategies for Parkinson’s disease.