Lidocaine attenuates lipopolysaccharide-induced inflammatory responses in microglia.

摘要: Abstract Background Lidocaine has been used as a local anesthetic with anti-inflammatory properties, but its effects on neuroinflammation have not well defined. In the present study, we investigated prophylactic of lidocaine lipopolysaccharide (LPS)-activated microglia and explored underlying mechanisms. Materials methods Microglial cells were incubated or without 1 μg/mL LPS in presence absence lidocaine, p38 mitogen–activated protein kinase (p38 MAPK) inhibitor (SB203580), nuclear factor-kappa B (NF-κB) (pyrrolidine dithiocarbamate), small interfering RNA. The expression levels inflammatory mediators, such monocyte chemotactic 1, nitric oxide, prostaglandin E2, interleukin 1β, tumor necrosis factor α measured using enzyme-linked immunosorbent assays real-time polymerase chain reaction. effect NF-κB MAPK activation was evaluated assays, Western blot analysis, electrophoretic mobility shift assay. Results (≥2 μg/mL) significantly inhibited release LPS-activated microglia. Treatment also phosphorylation translocation p50/p65, increased kappa B-α. Furthermore, our study shows that LPS-induced mediators suppressed by SB203580, pyrrolidine dithiocarbamate, Conclusions Prophylactic treatment inhibits from microglia, these may be mediated blockade signaling pathways.