Related Experiment Video
Updated: Jul 27, 2025
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
Published on: March 21, 2021
Monotropein alleviates sepsis-elicited acute lung injury via the NF-κB pathway
1Department of Infectious Diseases, Nanping First Hospital affiliated to Fujian Medical University, Nanping, Fujian, China.
Objectives:
To address the effect and mechanism of Monotropein (Mon) on sepsis-induced acute lung injury (ALI).
Methods:
ALI model was established by lipopolysaccharide (LPS)-stimulated mouse lung epithelial cell lines (MLE-12) and cecal ligation and puncture (CLP)-treated mice, respectively. The function of Mon was examined by cell counting kit-8 (CCK-8), pathological staining, the pulmonary function examination, flow cytometry, enzyme-linked immunosorbent assay, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labellingand western blot.
Results:
Mon increased the LPS-reduced viability but decreased the LPS-evoked apoptosis rate in MLE-12 cells. Mon suppressed the concentrations and protein expressions of proinflammatory factors, and the expressions of fibrosis-related proteins in LPS-challenged MLE-12 cells compared with LPS treatment alone. Mechanically, Mon downregulated the levels of NF-κB pathway, which was confirmed with the application of the receptor activator of nuclear factor-κB ligand (RANKL). Correspondingly, RANKL reversed the ameliorative effect of Mon on the proliferation, apoptosis, inflammation and fibrosis. Moreover, Mon improved the pathological manifestations, apoptosis, the W/D ratio and pulmonary function indicators in CLP-treated mice. Consistently, Mon attenuated inflammation, fibrosis and NF-κB pathway in CLP-treated mice.
Conclusion:
Mon inhibited apoptosis, inflammation and fibrosis to alleviate sepsis-evoked ALI via the NF-κB pathway.
