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Sinapic Acid Reduces Hypoxia-Induced Cell Damage in Hep-2 Cells by Regulating TRPM2 Channel Activation
Halil İbrahim Altıner1, Tarık Yağcı1, Ramazan Çınar2
1Department of Otorhinolaryngology, Faculty of Medicine, Bilecik Seyh Edebali University, Bilecik, Türkiye.
Journal of Biochemical and Molecular Toxicology
|June 25, 2026
Summary
Sinapic acid (SPA) protects laryngeal cancer cells from hypoxia-induced damage by reducing oxidative stress and inflammation. SPA modulates the TRPM2 channel, decreasing calcium overload and cell death, showing therapeutic potential for laryngeal squamous cell carcinoma.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Hypoxia (HPX) is a key factor in laryngeal squamous cell carcinoma (LSCC) pathogenesis, causing mitochondrial dysfunction, oxidative stress, inflammation, and calcium dysregulation.
- The TRPM2 channel is implicated in mediating hypoxia-induced calcium overload and cell death in LSCC.
- Sinapic acid (SPA), a natural phenolic compound, possesses antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the protective effects of sinapic acid (SPA) against hypoxia-induced injury in Hep-2 cells (LSCC model).
- To determine if SPA's protective mechanisms involve the modulation of the TRPM2 channel.
- To evaluate SPA's impact on oxidative stress, inflammation, and calcium homeostasis.
Main Methods:
- Hep-2 cells were subjected to cobalt chloride (CoCl2)-induced hypoxia and treated with varying concentrations of SPA.
- Assessed cell viability, oxidative stress markers (MDA, GSH, ROS), intracellular calcium levels, mitochondrial membrane potential, and pro-inflammatory cytokines (IL-1β, TNF-α).
- Evaluated TRPM2 expression, PI-positive cell death, and the effects of co-treatment with the TRPM2 inhibitor 2-APB.
Main Results:
- Hypoxia significantly reduced cell viability, increased oxidative stress and inflammation, depolarized mitochondria, and elevated TRPM2-dependent calcium influx.
- SPA treatment restored GSH levels, decreased MDA and ROS, suppressed cytokine production, stabilized mitochondrial membrane potential, and reduced TRPM2 upregulation and calcium overload.
- Co-treatment with SPA and 2-APB resulted in the most significant reduction in cell death, indicating synergistic protective effects.
Conclusions:
- Sinapic acid (SPA) effectively mitigates hypoxia-induced cytotoxicity in LSCC cells.
- SPA exerts its protective effects via antioxidative, anti-inflammatory, and TRPM2-modulating mechanisms.
- SPA demonstrates significant potential as a therapeutic agent for laryngeal squamous cell carcinoma.