It is widely diffused the role of melatonin as cell protection agent in both in vivo and in vitro models. Among the effects already described are the inhibition of apoptosis and neurodegeneration in different cell types (Luchetti et al., 2010), including hippocampal neurons stimulated by neurotoxin in vivo (Yalcin et al., 2004), cerebellar neurons after intracerebroventricular injection of endotoxin (Pinato et al, 2013), neuroblastoma cells (Choi et al., 2008). Furthermore, melatonin protect cells from oxidative stress (Herruzo Solis and Solis Munos, 2009; Esposito and Cuzzocrea, 2010; Cuesta et al 2011 ) or decreasing the aging effects (Srinivasan et al., 2005; Perreau et al, 2007;. Pizza et al, 2011). On the other hand, it is well known that melatonin potentiates the deficit and brain damage, neurodegeneration observed after stroke (Manev et al., 1996). Despite strong evidence that melatonin has neuroprotective effects, the mechanisms involved have not yet been clarified. Given the beneficial effects of exogenous melatonin in neurodegeneration that affects specific brain areas such as Alzheimer's and Parkinson (Reiter, 1998) another factor to be investigated would be the possible difference in melatonin action in specific brain areas. In this study, we aimed to investigate the effect of pretreatment with melatonin on cultures of cells from different brain areas challenged by TNF through the analysis of apoptosis and molecules involved in the inflammatory pathway.
News published in Agência FAPESP Newsletter about the scholarship: