Nicorandil mitigates glutamate excitotoxicity in primary cultured neurons

Abstract

Excitotoxicity, caused by the excessive release of glutamate, leads to the activation of the apoptotic process, making it a crucial factor in age-related neurodegenerative diseases. The aim of this study was to investigate the potential of nicorandil to prevent glutamate excitotoxicity and reduce oxidative stress in the brain by analyzing the effects of nicorandil on primary cortex neurons. The study used primary neuron cultures from newborn Sprague-Dawley rats to examine the impact of nicorandil on cell viability, Superoxide Dismutase, Catalase, Glutathione activity, Malondialdehyde levels, total antioxidant capacity, and total antioxidant status of neurons subjected to glutamate-induced excitotoxicity. Nicorandil at varying concentrations was introduced in the culture to assess its protective effects on the neurons. The results showed that nicorandil significantly improved cell viability and total antioxidant capacity levels and reduced total antioxidant status values in a concentration-dependent manner. These findings indicate that nicorandil effectively prevented glutamate excitotoxicity by reducing oxidative stress. The study suggests that nicorandil holds the potential for treating neurodegenerative diseases caused by glutamate excitotoxicity. This study is the first to report the potential of nicorandil to inhibit oxidative stress and prevent glutamate excitotoxicity in primary neurons, providing a basis for further exploration of the clinical application of nicorandil in neurodegenerative diseases.