Resveratrol Reduces Hypoxia-Caused Increases of Apoptosis and Oxidative Neurotoxicity via TRPA1 Cation Channel Suppression in Glioblastoma Cells

Authors : Kemal Ertilav

Pages : 382-389

Doi:10.26453/otjhs.1773319

View : 66 | Download : 127

Publication Date : 2025-12-20

Article Type : Research Paper

Abstract :Objective: Hypoxia (HPX) increases the amount of Ca2+ influx, apoptosis, and harmful free reactive oxygen species (ROS) in the brain and neurons. Resveratrol (RES) has been shown to reduce these increases in ROS-damaged neuronal cells by inhibiting voltage-gated Ca2+ channels. The aim of the study was to ascertain whether RES could also inhibit the elevated ROS and apoptosis induced by HPX in SH-SY5Y glioblastoma cells via inhibiting TRPA1. Materials and Methods: In the SH-SY5Y, four primary groups were induced as control, RES (50 µM for 24h), HPX (200 µM CoCl2 for 24h), and HPX + RES. Results: While the incubations of the TRPA1 antagonist (AP-18) and RES decreased the HPX-mediated upregulations of apoptotic (caspase -3, -8, and -9) and oxidants (ROS, mitochondrial dysfunction, and lipid peroxidation) concentrations, the TRPA1 agonist (cinnamaldehyde) stimulation further increased these concentrations. The RES increased viable cell percentage, glutathione concentration, and glutathione peroxidase activity, all of which were diminished by HPX. Conclusions: The concentrations of HPX-induced neuronal apoptosis and mitochondrial oxidative stress were reduced by RES treatment through TRPA1 inhibition. It seems that RES is a potential treatment option for HPX-induced mitochondrial oxidative neuronal injury.
Keywords : Apoptozis, hipoksi, mitokondriyal oksidatif stres, resveratrol, TRPA1 kanalı

ORIGINAL ARTICLE URL