Objective:To explore the therapeutic effect and mechanism of myricetin on disseminated intravascular coagulation (DIC).Methods:The DIC model was established by injection of 60 mg/kg LPS in KM mice,and the treatment groups were injected myricetin with different concentrations (25 or 50 mg/kg) 30 min before the model was established.Both coagulation indicators and organ function were tested,including PT,APTT,fibrinogen,AST,ALT,BUN and tissue section.In vitro,the inflammatory model of RAW 264.7 macrophage cells were established by 10 μg/mL LPS.The treatment group was treated with 50 μmol/mL myricetin for 30 min before LPS,and the expression of TNF-α and p-NF-κB was detected,further to explore the therapeutic mechanism.Results:LPS-induced DIC led to a reduction of fibrinogen and a rise of PT,APTT,AST,ALT,BUN levels,but the treatment of myricetin significantly inhibited these abnormalities.Histopathology analysis also revealed that myricetin remarkably protected the liver and renal damage.In vitro,the expression of TNF-α and p-NF-κB induced by LPS was repressed by myricetin.Conclusions:This study provides new insights into the protective effects of myricetin in LPS-induced DIC by anticoagulant and anti-inflammatory via suppressing the activation of p-NF-κB which decreased TNF-α level.