Efeito neurorreparador da sarcosina no modelo de isquemia cerebral focal

Abstract

Annually, approximately 17 million individuals worldwide suffer from a Stroke (Cerebrovascular Accident), a condition that can result in permanent neurological sequelae or even death. Cerebral ischemia, the primary cause of these events, is characterized by a reduction in cerebral blood flow, which can occur in a localized or generalized manner. In this context, the present study aimed to evaluate the neuroprotective and neuroreparative effects of sarcosine by investigating its influence on neuronal regeneration in animal models subjected to middle cerebral artery occlusion (MCAO). For this purpose, the animals received intraperitoneal treatment with sarcosine at doses of 125 mg/kg, 250 mg/kg, and 500 mg/kg over a period of 28 days following the induction of the MCAO model. Motor evaluation was conducted through the Limb Clasping and Cylinder behavioral tests on days 7, 14, and 28 post-inductions. Additionally, the Object Location Task (OLT) and Novel Object Recognition Test (NORT) memory tests were conducted on the 28th day. We performed molecular analysis using the Western Blotting technique to assess the expression levels related to the glycine transporter (GlyR), glycine transporters (Glyt1 and Glyt2), NMDA receptor subunits (GluN1, GluN2A, and GluN2B), proteins associated with cell survival pathways (CaMK II, CaMK IV, CREB), proteins associated with brain-derived neurotrophic factor BDNF, and TrKb. The results demonstrated that sarcosine improves motor and cognitive deficits in animals subjected to ischemia. It is concluded that sarcosine treatment shows promising neuroprotective potential in the context of ischemic stroke induced in an animal model.