Schisantherin-A Alleviates Lipopolysaccharide-Induced Inflammation and Apoptosis in WI-38 Cells

Abstract

Schisantherin A, a dibenzocyclooctadiene lignan, isolated from the fruit of Schisandra sphenanthera has been widely used to exert anti-inflammatory or antioxidant activities in sepsis associated acute kidney injury and lipopolysaccharide associated acute respiratory distress syndrome. However, the protective effects of Schisantherin A against acute pneumonia in lipopolysaccharide-induced WI-38 remain to be explored. To this end, WI-38 cells were treated with lipopolysaccharide to establish an acute pneumonia model and evaluate the effect of Schisantherin A. The data show an increase in apoptosis and decrease in cell viability by lipopolysaccharide treatment that was reversed by Schisantherin A. Also, Schisantherin A dose dependently attenuated lipopolysaccharide-induced increase in proinflammatory cytokines. Lastly, expression of p65, p38 proteins, extracellular-signal-regulated kinase, and Jun N-terminal protein kinase phosphorylation were upregulated by lipopolysaccharide and decreased by Schisantherin A. In conclusion, Schisantherin A demonstrates anti-inflammatory and antiapoptotic roles in lipopolysaccharide induced WI-38 cells through inactivation of nuclear factor-kappa B/mitogen activated protein kinase pathway.