Remimazolam attenuates inflammation in bronchopneumonia through the inhibition of NLRP3 activity by PDPK1 ubiquitination

Abstract Bronchopneumonia is the most common pneumonia in childhood. Therefore, we tested the effects of Remimazolam presented Bronchopneumonia and its possible mechanisms. Phillygenin increased survival rate, reduced W/D ratio, and lung injury score, and inhibited IL‐1β, IL‐6, TNF‐α, and INF‐γ levels in mice model of bronchopneumonia. Remimazolam induced PDPK1 and p‐AKT protein expressions, and suppressed NLRP3 protein expression in lung tissue of mice model. In vitro model, Remimazolam also induced PDPK1 and p‐AKT protein expressions, and suppressed NLRP3 protein expression. Remimazolam also inhibited inflammation levels in vitro model. PDPK1 inhibitor, PHT‐427 (100 mg/kg) reduced survival rate, increased W/D ratio and lung injury score, and promoted inflammation levels in mice model of bronchopneumonia by treated with Remimazolam. PHT‐427 suppressed PDPK1 and p‐AKT protein expressions and induced NLRP3 protein expression in mice model of bronchopneumonia by treated with Remimazolam. Remimazolam interlinked PDPK1 protein. Remimazolam increased the expressions of PDPK1 and p‐AKT in vitro model. Remimazolam reduced PDPK1 ubiquitination in vitro model.