LAUSR

Abstract Propofol, one of the most commonly used intravenous anesthetic agents, has been reported to have anti‐inflammatory property. However, the anti‐allergic inflammation effect of propofol and its underlying molecular mechanisms have not been elucidated. In the present study, we aim to investigate the roles of NF‐kB activation in propofol anti‐asthma effect on OVA‐induced allergic airway inflammation in mice. In a standard experimental asthma model, Balb/c mice were sensitized with ovalbumin, treated with propofol (50,100,150 mg/kg) or a vehicle control 1 h before OVA challenge. Blood samples, bronchoalveolar lavage fluid (BALF) and lung tissues were harvested after measurement of airway hyperresponsiveness. Results revealed that propofol not only significantly inhibit airway hyperresponsiveness, but also inhibited the production of Th2 cytokines, NO, Ova‐specific IgE and eotaxin. Histological studies indicated that propofol significantly attenuated OVA‐induced inflammatory cell infiltration in the peribronchial areas and mucus hypersecretion. Meanwhile, our results indicated that propofol was found to inhibit NF‐kB activation in OVA‐Induced mice. Furthermore, propofol significantly reduced the TNF‐&agr;‐induced NF‐kB activation in A549 cells. In conclusion, our study suggested that propofol effectively reduced allergic airway inflammation by inhibiting NF‐kB activation and could thus be used as a therapy for allergic asthma. HighlightsT helper type 2 lymphocytes play a pivotal role in the pathogenesis process of allergic asthma.Propofol can ameliorate airway inflammation in ovalbumin (OVA)‐Induced allergic asthma mice.The mechanism relies on NF‐&kgr;B signaling.