Efeitos do ácido láurico nas alterações locomotoras e neuroquímicas induzidas pelo haloperidol em ratos

• Ano de defesa: 2025
• Autor(a) principal: Nascimento, Jordânia Magalhães do
• Orientador(a): Aguiar, Lissiana Magna Vasconcelos
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Área do conhecimento CNPq: Biotecnologia
• Link de acesso: http://repositorio.ufc.br/handle/riufc/80877

Parkinson's disease (PD) is an age-related progressive neurodegenerative disease. Treatment with l-dopa is considered the gold standard treatment for PD, however, its long-term use is associated with significant side effects. Therefore, there is an incessant search for new substances capable of relieving motor symptoms and decreasing the progression of neuronal degeneration. Lauric acid (AL) is a saturated fatty acid that has proven to be very promising in research related to central nervous system (CNS) injury. Thus, the present study aimed to evaluate the neuroprotective effect of lauric acid alone (AL) and its combination with Ldopa, against the neurodegeneration caused by haloperidol. Male Wistar rats, adults, who received treatment with lauric acid in doses (5, 10 and 20 mg/kg) alone, or with the association (AL + l-dopa), or with saline (controls) by gavage, for 14 days. From the seventh day of the beginning of treatment, the animals received haloperidol 1.0 mg/kg/day via i.p. After treatment, the animals were subjected to behavioral tests (dyskinesia and catalepsy test). At the end of the treatment, the animals were sacrificed and the brain areas of interest to the research were removed for neurochemical assays (TBARS, nitrite and GSH). The results revealed that only treatment with lauric acid at the lowest dose (5 mg/kg) was able to significantly reduce haloperidol-induced catalepsy after 15 minutes. Treatment with LA only with the highest dose (20 mg/kg), alone or associated with L-dopa were able to prevent this effect. The orofacial movements of tongue protusion were significantly reduced with treatment with AL in all doses, and also with treatment with L-dopa alone and associated with LA. The results that there was an increase in MDA levels in the hippocampus, striated body and prefrontal cortex caused by haloperidol, and treatment with AL and L-dopa were able to reverse this increase, however only the highest dose was effective in the striated body. AL and L-dopa alone and in association were able to reverse the increase in nitrite in the brain areas in all doses tested. Treatment with haloperidol reduced endogenous GSH levels in the hippocampus striated body and prefrontal cortex, however, only treatment with AL at doses 10 and 20 mg/kg were able to reverse this reduction in the hippocampus, as well as treatment with L-dopa. In the striated body and prefrontal cortex there were no significant changes.