This is supported further by the findings that LPS-induced expression of HMGB1, a semi-late (expressed 4 hrs after LPS challenge), and late acting proinflammatory cytokine [13], [30] which contributes to endotoxin-induced ALI and sepsis-associated lethality [10], [11], [13], was significantly inhibited by OroA (iv) administered 1 hr or 6 hrs after LPS challenge. This evidence concerns the gene HMGB1 and acute respiratory distress syndrome.