RT info:eu-repo/semantics/article
T1 Anti-neuroinflammatory potential of a Nectandra angustifolia (Laurel amarillo) ethanolic extract
A1 Crescitelli, María Carla
A1 Simón de la Fuente, Inmaculada
A1 Ferrini, Leandro
A1 Calvo Vecino, Hugo
A1 Torres, Ana María
A1 Cabero, Isabel
A1 Macías Panedas, Mónica
A1 Rauschemberger, Maria B.
A1 Aguirre, Maria V.
A1 Rodríguez, Juan Pablo
A1 Hernández Garrido, Marita
A1 Nieto, Maria Luisa
K1 Microglia
K1 Neurosciences
K1 Immunology
K1 Neurology
K1 Neuroinflammation
K1 Central nervous system - Diseases
K1 Sistema nervioso central - Enfermedades
K1 Plant extracts
K1 Phagocytosis
K1 Cell death
K1 Células - Muerte
K1 Food science
K1 Biochemistry
K1 Clinical biochemistry
K1 Molecular biology
K1 2490 Neurociencias
K1 2412 Inmunología
K1 3205.07 Neurología
K1 3309 Tecnología de Los Alimentos
K1 2302 Bioquímica
K1 2415 Biología Molecular
AB Microglia, the resident macrophage-like population in the CNS, plays an important role in the pathogenesis of many neurodegenerative disorders. Nectandra genus is known to produce different metabolites with anti-inflammatory, anti-oxidant and analgesic properties. Although the species Nectandra angustifolia is popularly used for the treatment of different types of inflammatory processes, its biological effects on neuroinflammation have not yet been addressed. In this study, we have investigated the role of a Nectandra angustifolia ethanolic extract (NaE) in lipopolysaccharide (LPS)-induced neuroinflammation in vitro and in vivo. In LPS-activated BV2 microglial cells, NaE significantly reduced the induced proinflammatory mediators TNF-α, IL-1β, IL-6, COX-2 and iNOS, as well as NO accumulation, while it promoted IL-10 secretion and YM-1 expression. Likewise, reduced CD14 expression levels were detected in microglial cells in the NaE+LPS group. NaE also attenuated LPS-induced ROS and lipid peroxidation build-up in BV2 cells. Mechanistically, NaE prevented NF-κB and MAPKs phosphorylation, as well as NLRP3 upregulation when added before LPS stimulation, although it did not affect the level of some proteins related to antioxidant defense such as Keap-1 and HO-1. Additionally, we observed that NaE modulated some activated microglia functions, decreasing cell migration, without affecting their phagocytic capabilities. In LPS-injected mice, NaE pre-treatment markedly suppressed the up-regulated TNF-α, IL-6 and IL-1β mRNA expression induced by LPS in brain. Our findings indicate that NaE is beneficial in preventing the neuroinflammatory response both in vivo and in vitro. NaE may regulate microglia homeostasis, not only restraining activation of LPS towards the M1 phenotype but promoting an M2 phenotype.
PB MDPI
SN 2076-3921
YR 2023
FD 2023
LK https://uvadoc.uva.es/handle/10324/69529
UL https://uvadoc.uva.es/handle/10324/69529
LA eng
NO Antioxidants, 2023, Vol. 12, Nº. 2, 232
NO Producción Científica
DS UVaDOC
RD 06-oct-2024