Efeitos do ácido clorogênico na modulação da sinalização purinérgica e perfil inflamatório em células microgliais expostas ao lipopolissacarídeo

• Ano de defesa: 2021
• Autor(a) principal: Mostardeiro, Vitor Bastianello
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Santa Maria; Brasil; Bioquímica; UFSM; Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica; Centro de Ciências Naturais e Exatas
• Palavras-chave em Português: Doença de Alzheimer; Células microgliais; Neuroinflamação; Neurodegeneração; Sistema purinérgico; Alzheimer’s disease; Microglial cells; Neuroinflammation; Neurodegeneration; Purinergic system; CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA
• Link de acesso: http://repositorio.ufsm.br/handle/1/23603

Neuroinflammation is a process associated with various neurodegenerative diseases, especially Parkinson’s and Alzheimer’s Disease. In the Central Nervous System (CNS), microglial cells are the most important macrophages and their activation is closely related to the inflammatory process seen in neurodegenerative diseases. The purinergic sysem also has a very intimate relationship with the inflammatory process and its components might be modulating inflammatory responses in the CNS. Chlorogenic Acid (CGA) is a natural product known for its antioxidant and anti-inflammatory activities that would be able to modulate the responses of the purinergic system, interfering with the neuroinflammatory process. Thus, this study aimed to investigate the possible in vitro therapeutic effects of CGA in a model involving the purinergic system and microglial cells (BV-2) exposed to lipopolysaccharide (LPS) (1 ug/mL) and treatment with an increasing concentration effect curve of CGA (0.5 to 300 uM), for 24 and 96 hours. Results show that CGA is able to modulate purinergic activity by restoring ATP hydrolysis levels to those of the control, and increasing the Adenosine breakdown. CGA also acted on the expression of purinergic receptors P2X7 and A2A, and greatly reducing the releases of the pro-inflammatory cytokine IL-1β. It was also verified that this compound reduced the ratio of migrated cells after LPS challenge at both times. Therefore, despite the restrictions of in vitro protocols, this work highlights the therapeutic potential of this natural product in the possible treatment of inflammation in the CNS.