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

瑞马唑仑通过 PDPK1 泛素化抑制 NLRP3 活性来减轻支气管肺炎的炎症

阅读:6
作者:Min Yang, Ling Li

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.

特别声明

1、本文转载旨在传播信息,不代表本网站观点,亦不对其内容的真实性承担责任。

2、其他媒体、网站或个人若从本网站转载使用,必须保留本网站注明的“来源”,并自行承担包括版权在内的相关法律责任。

3、如作者不希望本文被转载,或需洽谈转载稿费等事宜,请及时与本网站联系。

4、此外,如需投稿,也可通过邮箱info@biocloudy.com与我们取得联系。