Acanthamoeba genus amoebae can affect humans with diseases such as Granulomatous Amebic Encephalitis (GAE), a highly lethal neuroinfection. Several aspects about the disease still need to be elucidated. Animal models of GAE have allowed advances in these aspects. This work tested Wistar rats (Rattus norvegicus albinus) as an animal model of GAE. For this, 32 animals were infected with 1x10⁶ A. castellanii trophozoites, T4 genotype. Ameba recovery tests were carried out on plates of agar, vascular extravasation assays, behavioral tests and histopathological technique with H/E staining. Data were submitted to linear regression analysis, one-way ANOVA and Tukey's test, performed in the GraphPad Prism® 8.0 program, with a significance level of p<0.05. The results revealed the efficiency of the model. There was recovery of amoebae from the liver, lungs and brain of infected animals, significant encephalic vascular extravasation and behavioral changes in these animals, but not in the control animals. However, not all infected animals showed positive histopathology for the analyzed organs. The nervous tissue was the least affected, demonstrating the role of the BBB in the defense of the CNS. Supported by the demonstrated evidence, we confirm the difficulty, but also the feasibility of using rats as an animal model of GAE.

The use of pesticides such as rotenone can lead to toxicity, dysfunction and neuronal death in humans. The Copaifera Reticulata Ducke Oil-Resin (CPOR) is widely used by the natives of the Amazon, however, studies on its potential neuroprotective effect are lacking. This study investigated the cytoprotective effect of CPOR on total cell cultures of the ventral midbrain (VMC), hippocampus (HC) and cerebral cortex (CCC) exposed to rotenone at different concentrations. The total cell cultures of VMC, HC and CCC were exposed for 72 or 24 hours to rotenone, CPOR and rotenone + CPOR. Cell viability was measured using the MTT test and compared using one-way ANOVA. Exposure to rotenone reduced the cell viability of CMV, HC and CCC. Exposure to CPOR reduced the cell viability of CMV. The cell viability of CMV exposed simultaneously to rotenone and CPOR was higher compared to rotenone alone. The cell viability of HC exposed simultaneously to rotenone and CPOR was higher than that exposed to rotenone. CMVs are more vulnerable to rotenone toxicity and more sensitive to CPOR. Considering simultaneous exposure, CPOR revealed a possible neuroprotective effect against rotenone damage only for VMC and HC.