casticin and Acute-Lung-Injury

Casticin, an active compound isolated from Vitex Fructus, has been reported to have anti-inflammatory effects in previous studies. The present study was designed to evaluate the protective effects of casticin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and clarify the underlying mechanisms. ALI was induced by intratracheal instillation of LPS. Casticin was administrated 1h before or after LPS challenge. The results showed that casticin decreased LPS-induced lung histopathological changes, MPO activity, and lung wet/dry weight ratio. Casticin also inhibited the numbers of inflammatory cells and the levels of inflammatory cytokines TNF-α, IL-6, and IL-1β production. Furthermore, casticin suppressed LPS-induced NF-κB activation, and NLRP3, ASC, and caspase-1 expression. In conclusion, the results suggested that casticin had a protective effect against LPS-induced ALI. Casticin protected against LPS-induced ALI by inhibiting inflammatory cytokines production through the inhibition of NF-κB and NLRP3 signaling pathways.

Topics: Acute Lung Injury; Animals; Apoptosis Regulatory Proteins; CARD Signaling Adaptor Proteins; Caspase 1; Flavonoids; Gene Expression Regulation; Gene Expression Regulation, Enzymologic; Lipopolysaccharides; Lung; Male; Mice; Mice, Inbred BALB C; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; Peroxidase; Signal Transduction