Halenia

1-Hydroxy-2,3,5-trimethoxyxanthone (HM-1) exhibits vasodilator action through an endothelium-dependent mechanism involving NO and an endothelium-independent mechanism by inhibiting Ca(2+) influx via L-type voltage-operated Ca(2+) channels. A minor contribution to HM-1's effects may stem from inhibiting protein kinase C-mediated release of intracellular Ca(2+) stores. At 1 µg/mL, HM-1 effectively inhibits osteoclast differentiation in co-cultures with mouse osteoblastic calvarial and bone marrow cells and protects mice from acute lung injury induced by lipopolysaccharide (LPS), likely by increasing IκB-α protein expression and suppressing inducible nitric oxide synthase and cyclooxygenase-Ⅱ protein expression.