Inhibitory effects of coumarin and acetylene constituents from the roots of Angelica furcijuga on d-galactosamine/lipopolysaccharide-induced liver injury in mice and on nitric oxide production in lipopolysaccharide-activated mouse peritoneal macrophages

The methanolic extract (200 mg/kg, p.o. and i.p.), principal coumarin constituents (isoepoxypteryxin, anomalin, and praeroside IV), and a polyacetylene constituent (falcarindiol) (25 mg/kg, i.p.) from the roots of Angelica furcijuga protected the liver injury induced by d-galactosamine (d-GalN)/lipopolysaccharide (LPS) in mice. In in vitro experiments, coumarin constituents (hyuganins A–D, anomalin, pteryxin, isopteryxin, and suksdorfin) and polyacetylene constituents [(−)-falcarinol and falcarindiol] substantially inhibited LPS-induced NO and/or TNF-α production in mouse peritoneal macrophages, and isoepoxypteryxin inhibited d-GalN-induced cytotoxicity in primary cultured rat hepatocytes. Furthermore, hyuganin A, anomalin, and isopteryxin inhibited the decrease in cell viability by TNF-α in L929 cells.

The methanolic extract, principal coumarin constituents (isoepoxypteryxin, anomalin, and praeroside IV), and a polyacetylene constituent (falcarindiol) from the roots of Angelica furcijuga protected the liver injury induced by d-galactosamine (d-GalN)/lipopolysaccharide (LPS) in mice. In in vitro experiments, coumarin constituents (hyuganins A–D, anomalin, pteryxin, isopteryxin, and suksdorfin) and polyacetylene constituents [(−)-falcarinol and falcarindiol] substantially inhibited LPS-induced NO and/or TNF-α production in mouse peritoneal macrophages, and isoepoxypteryxin inhibited d-GalN-induced cytotoxicity in primary cultured rat hepatocytes. Furthermore, hyuganin A, anomalin, and isopteryxin inhibited the decrease in cell viability by TNF-α in L929 cells.Figure optionsDownload as PowerPoint slide