Implications of nitrosative stress in apoptotic cascades mediated by pro-inflammatory cytokines in immature neurons

Abstract

The inflammatory response is essential for survival in response to tissue injury or infection, but it can also cause neuronal damage [1]. In fact, pro-inflammatory cytokines, as well as nitric oxide (NO), are known as mediators of neuronal apoptosis [2,3]. Although apoptosis occurs physiologically in the brain during the period of the growth spurt, an increase in the number of neurons undergoing apoptosis may produce neuropathological sequelae [4]. Therefore, the aim of the present study was to: (i) deepen characterize the mechanisms of neuronal apoptosis upon cytokine exposure in neuronal immature cells; and (ii) investigate the role of NO as a determinant.