Pregabalin protected cisplatin-induced oxidative neurotoxicity in neuronal cell line

Cisplatin (CSP) is used treatment of several cancers. However, it has also adverse effect through excessive reactive oxygen species production and activation of TRPV1 channel activation in neurons. Pregabalin (PGAB) has antioxidant and calcium channel blocker actions in neurons. I have investigated protective role of PGAB against the adverse effects of CSP in DBTRG neuronal cells. The neuronal cells were divided into four groups as control group, PGAB group (500 M for 24 1 hrs), CSP group (25 M for 24 hrs), and PGAB+CSP combination group. CISP-induced decrease of cell viability, glutathione peroxidase and glutathione level in the cells were increased in the neurons by PGAB treatment. However, CSP-induced increase of apoptosis, Ca2+ fluorescence intensity, TRPV1 current densities through the increase mitochondrial oxidative stress were decreased in the neurons by PGAB treatment. In conclusion, CSP-induced increases in mitochondrial ROS and cell death levels in the neuronal cells were decreased through the decrease of TRPV1 activation with the effect of PGAB treatment. CSP-induced drug resistance in the neurons might be reduced by PGAB treatment.