Morusin attenuates LPS-induced inflammation and oxidative stress in lung epithelial cells by inhibiting NLRP3 inflammasome activation.

Abstract

Acute lung injury (ALI) is a pulmonary disorder characterized by severe lung tissue damage and inflammation. Morusin (a flavone, a type of flavonoid; C₂₅H₂₄O₆), a flavonoid isolated from mulberry root bark, possesses notable anti-inflammatory and antioxidant properties. However, its regulatory effects on ALI progression remain unclear. This study aimed to investigate whether morusin could mitigate the development of ALI. Morusin was shown to enhance cell viability and reduce apoptosis in lipopolysaccharide (LPS)-stimulated A549 cells. Furthermore, morusin alleviated inflammation by decreasing the levels of interleukin-1β (IL-1β), IL-6, and prostaglandin E2 (PGE2) in LPS-challenged A549 cells. In addition, morusin effectively reduced oxidative stress in these cells. Mechanistically, morusin was found to suppress the activation of NLRP3 (nucleotide-binding domain, leucine rich-containing family, pyrin domain containing 3) inflammasome in LPS-stimulated A549 cells. Finally, this study demonstrated for the first time that morusin ameliorates LPS-induced inflammation and oxidative stress in lung epithelial cells by inhibiting both nuclear factor kappa B signaling pathway and NLRP3 inflammasome activation. However, this project was limited to cell experiments, and no animal experiments or clinical verifications were conducted. Our findings suggest that morusin could serve as a promising therapeutic agent for the treatment of ALI.