Protective effects of zingerone against bisphenol-A induced oxidative stress and apoptosis in SH-SY5Y cells: the role of TRPM2 channel
Molecular Biology Reports, cilt.53, sa.1, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 53 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s11033-026-12074-5
- Dergi Adı: Molecular Biology Reports
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Anahtar Kelimeler: Bisphenol A, Neuroprotection, Oxidative stress, TRPM2 channel, Zingerone
- Van Yüzüncü Yıl Üniversitesi Adresli: Evet
Özet
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