MELATONIN MODULATES NEUROINFLAMATION, ASTROGLIOSIS AND PROTECTS AGAINST OXIDATIVE STRESS IN EXPERIMENTAL CEREBRAL MALARIA

Exacerbated microglial activation induces neuroinflammation, reactive astrogliosis, from the release of pro-inflammatory cytokines, and oxidative stress mediated by the production of elevated levels of reactive oxygen species. In cerebral malaria (CM), the main complication of Plasmodium falciparum infection, these events are related to the pathogenesis of the disease. The presence of Plasmodium in the central nervous system induces damage to the blood-brain barrier and changes at cellular level that results in neuronal death mediated by mechanisms involving neuroinflammation, oxidative stress and astrogliosis. Our previous results demonstrated that melatonin (mel), a hormone with anti-inflammatory and antioxidant properties, protected against blood-brain barrier breakdown and cell loss on the cortex of infected animals in experimental model of cerebral malaria (ECM). Therefore, we investigated the mechanisms involved in the neuroprotection of melatonin, highlighting the possible modulation of neuroinflammation and oxidative stress.