RESUMO
Ferulic acid (FA) is a natural compound that expresses antioxidant and anti-inflammatory activities. Microglial cells are innate immune cells that reside within the central nervous system (CNS). Activated microglia mediated neuronal immunity contributes to the neurodegeneration associated with Alzheimer's disease. In this study, we investigated the inhibitory effect of FA on neuroinflammation in BV-2 microglial cells induced by lipopolysaccharides (LPS). Our study showed that FA significantly suppressed the production of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin-1ß (IL-1ß), and decreased induced type II nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein in LPS-stimulated BV-2 microglia cells in a dose dependent manner. We hypothesized that this was achieved by suppressing the protein level of Toll-like receptor 4 (TLR4).
Assuntos
Doença de Alzheimer/imunologia , Ácidos Cumáricos/farmacologia , Lipopolissacarídeos/imunologia , Microglia/imunologia , Doença de Alzheimer/tratamento farmacológico , Animais , Linhagem Celular , Dinoprostona/imunologia , Humanos , Camundongos , Microglia/efeitos dos fármacos , Óxido Nítrico Sintase Tipo II/imunologiaRESUMO
OBJECTIVE: To study the inhibitory effect of Luteolin on LPS-induced BV-2 cell. METHODS: BV-2 cells were treated with LPS (0.1 microg/mL) for inflammation model; MTT assay was used to detect the viability of BV-2 cells; Nitric oxide (NO) was detected by the method of nitric acid reductase assay; Induce type II nitric oxide synthase (iNOS) enzyme activity was determined by type of nitric oxide synthase assay;TLR4 protein expression was examined by the Western Blot analysis. RESULTS: Luteolin significantly decreased the NO production and TLR4 protein expression as well as iNOS activity in LPS-activated microglial cell. CONCLUSION: LPS induced activation of microglia lead to inflammatory response and its mechanism may be related to inhibiting TLR4 signaling pathway.
Assuntos
Anti-Inflamatórios/farmacologia , Inflamação/prevenção & controle , Luteolina/farmacologia , Microglia/efeitos dos fármacos , Animais , Western Blotting , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Inflamação/induzido quimicamente , Inflamação/metabolismo , Lipopolissacarídeos/administração & dosagem , Lipopolissacarídeos/farmacologia , Camundongos , Microglia/metabolismo , Microglia/patologia , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase/metabolismo , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismoRESUMO
OBJECTIVE: To study the mechanism of baicalin on the cytokines of Th1/Th2 in murine model of asthma. METHODS: The murine model of asthma was induced by OVA. Different doses of baicalin were orally administered to the mice respectively. The spleen cells were cultured 3 days for the measurement of IFN-gamma, IL-4, IL-5 and IL-10 by ELISA. After 2 days of culture, the spleen cells were treated with Trizol for extraction of total RNA. The gene expressions of T-bet, GATA-3 and STAT-6 were analyzed by RT-PCR. RESULTS: The treatment with baicalin obviously decreased the production of IL-4 and IL-5 and the gene expression of GATA-3, STAT-6, but increased the production of IL-10. CONCLUSION: Baicalin may modulate the Th1/Th2 balance mainly by altering the gene expressions of GATA-3 and STAT-6 in vivo and increasing the production of IL-10.
