Propofol partially attenuates complete freund's adjuvant‐induced neuroinflammation through inhibition of the ERK1/2/NF‐κB pathway

Peripheral inflammation in male C57BL/6 mice was induced by intraplantar injection of 20 μL complete freund's adjuvant (CFA) in the left hind paw. Mice were randomly divided into three groups: Sham, CFA, and propofol+CFA. Mechanical allodynia was assessed by von Frey analysis, and heat hyperalgesia was detected by exposure of the plantar surface to a beam of radiant heat. Propofol significantly attenuated the severity and duration of CFA‐induced pain hypersensitivity, heat hyperalgesia, and paw edema. Propofol inhibited CFA‐induced microglia activation, and markedly decreased CFA‐induced ionized calcium binding adapter molecule 1 (IBA‐1) expression. Propofol inhibited CFA‐induced expression of p‐extracellular signal‐regulated kinase1/2 (p‐ERK1/2) and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) p65, as demonstrated by Western blot analysis. In addition, 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide assays indicated that propofol had no cytotoxic effect on BV2 microglia cells. Reverse transcription‐quantitative‐polymerase chain reaction and enzyme‐linked immunosorbent assay results demonstrated that propofol attenuates CFA‐induced tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐6, and IL‐1β production in the spinal cord as well as in BV2 cells. Taken together, these results demonstrate that propofol attenuates CFA‐induced neuroinflammation (TNF‐α, IL‐6, and IL‐1β expression) through a mechanism that involves activation of ERK1/2/NF‐κB signaling pathway. Propofol attenuates complete freund's adjuvant (CFA)‐induced neuroinflammation (tumor necrosis factor‐α [TNF‐α], interleukin‐6 [IL‐6], and IL‐1β expression) through a mechanism that involves activation of extracellular signal‐regulated kinase1/2/nuclear factor kappa‐light‐chain‐enhancer of activated B cells (ERK1/2/NF‐κB) signaling pathway.