Research Information System
NEUROCHEMICAL JOURNAL, vol.19, no.4, pp.942-953, 2026 (SCI-Expanded)
Abstract—Current treatments for glioblastoma (GBM), defined as the brain and spinal cord tumour with the
worst prognosis in adults, do not sufficiently improve the prognosis. Therefore, there is a clear need to investigate the possible molecular pathways of tumour proliferation and metastasis and new strategic approaches
for its treatment. In this study, we aimed to elucidate the synergistic chemotherapeutic activity of gallic acid
(GA) with doxorubicin (DOX) in human glioblastoma tumour cells (DBTRG) and the molecular mechanisms of these effects. For this purpose, we investigated the stimulatory role of GA on DOX-induced human
glioblastoma tumour cell (DBTRG) death via TRPM2 channel activation. For the study, five groups were
formed from DBTRG cells as Control, GA (4O μM), DOX (1 μM), GA + DOX, and ACA + DOX (ACA,
25 μM). In the analyses made, Total Antioxidant/Oxidant/ (TAS and TOS) status, cell viability, lipid peroxidation levels, glutathione peroxidase (GSH-Px) and glutathione (GSH) enzyme activity, caspase activity,
reactive oxygen species (ROS), inflammation markers, Poly ADP Ribose Polymerase-1, (PARP-1), and
Transient Receptor Potential Melastatin 2 (TRPM2) levels in the cells were determined. DOX treatment
reduced TAS, GSH, GSH-Px, and cell viability levels while increasing inflammatory indicators, TOS, ROS,
MDA, caspase, PARP-1, and TRPM2 levels and causing DBTRG cell cytotoxicity. The treatment was even
more successful when GA and DOX were used together. In conclusion, the increase in cell death and ROS
levels mediated by TRPM2 activation in DOX DBTRG cells was further enhanced by GA treatment.