Scholarlink

Background <p>Bisphenol A (BPA) is a common environmental endocrine disruptor that causes oxidative stress and neuronal damage. However, the role of redox-sensitive ion channels, such as TRPM2, and potential protective interventions have not been thoroughly explored. This study provides novel mechanistic insight into TRPM2-mediated neuronal damage and highlights the potential of zingerone (ZG) as a natural therapeutic strategy against environmental neurotoxicity.</p> Methods <p>The cells were exposed to BPA (250 µM) with or without ZG (25 µM) for 24&#xa0;h. We assessed cell viability (CCK-8), oxidative stress parameters (MDA, ROS, GSH, and GSHPx), inflammatory cytokines (IL-1β, IL-6, and TNF-α), apoptotic caspases (3, 8, and 9), and TRPM2/PARP-1 expression using ELISA and Western blotting.</p> Results <p>Exposure to BPA significantly reduced cell viability and triggered oxidative imbalance, inflammation, and apoptosis, as well as upregulation of TRPM2. In contrast, co-treatment with ZG restored antioxidant defences, suppressed cytokine release, inhibited caspase activation, and downregulated PARP-1/TRPM2 signaling.</p> Conclusions <p> These results suggest that ZG protects against BPA-induced neuronal damage by regulating PARP-1/TRPM2-associated redox signalling pathways and provide further evidence for TRPM2's involvement in environmental neurotoxicity</p> Graphical abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Protective effects of zingerone against bisphenol-A induced oxidative stress and apoptosis in SH-SY5Y cells: the role of TRPM2 channel

  • 期刊论文

  • 发表日期：

    2026年6月3日

查看全文
  • Ramazan Çınar,
  • Cüneyt Çağlayan,
  • Mahmut Yardımcı,
  • Kenan Yıldızhan

摘要

Background

Bisphenol A (BPA) is a common environmental endocrine disruptor that causes oxidative stress and neuronal damage. However, the role of redox-sensitive ion channels, such as TRPM2, and potential protective interventions have not been thoroughly explored. This study provides novel mechanistic insight into TRPM2-mediated neuronal damage and highlights the potential of zingerone (ZG) as a natural therapeutic strategy against environmental neurotoxicity.

Methods

The cells were exposed to BPA (250 µM) with or without ZG (25 µM) for 24 h. We assessed cell viability (CCK-8), oxidative stress parameters (MDA, ROS, GSH, and GSHPx), inflammatory cytokines (IL-1β, IL-6, and TNF-α), apoptotic caspases (3, 8, and 9), and TRPM2/PARP-1 expression using ELISA and Western blotting.

Results

Exposure to BPA significantly reduced cell viability and triggered oxidative imbalance, inflammation, and apoptosis, as well as upregulation of TRPM2. In contrast, co-treatment with ZG restored antioxidant defences, suppressed cytokine release, inhibited caspase activation, and downregulated PARP-1/TRPM2 signaling.

Conclusions

These results suggest that ZG protects against BPA-induced neuronal damage by regulating PARP-1/TRPM2-associated redox signalling pathways and provide further evidence for TRPM2's involvement in environmental neurotoxicity

Graphical abstract