Propofol Alleviates LPS-Induced Acute Lung Injury by Inhibiting Pulmonary Alveolar Epithelium Pyroptosis

Abstract

This study established experimental models of acute lung injury (ALI) both in vitro, using human alveolar epithelial cells, and in vivo, using murine models, with ALI induced by lipopolysaccharide (LPS). Propofol was administered to the animal models, and its effects on alveolar epithelial cell damage, lung tissue pathology, and inflammatory mediator levels were evaluated to assess its potential protective role against lung injury. The results showed that LPS-induced reactive oxygen species (ROS) played a central role in the development of ALI in both the cell and animal models, triggering pyroptosis of alveolar epithelial cells. This, in turn, led to the release of pro-inflammatory cytokines, exacerbating the lung injury. Importantly, propofol was found to reduce LPS-induced ALI by inhibiting ROS production and modulating key proteins involved in the pyroptosis pathway. These findings offer new insights into the mechanisms underlying ALI, providing a basis for the development of clinical treatments and suggesting promising therapeutic strategies for ALI patients.