Monotropein alleviates sepsis-elicited acute lung injury via the NF-κB pathway.

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.

Down-regulation of microRNA-155 suppressed Candida albicans induced acute lung injury by activating SOCS1 and inhibiting inflammation response.

Acute lung injury caused by Candida albicans could result in high mortality and morbidity. MicroRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) have been believed to play a key in the regulation of inflammatory response. Whether miR-155/SOCS1 axis could regulate the acute lung injury caused by C.