Objective:To investigate whether atractylenolide Ⅰ(ATL-Ⅰ) has protective effect on lipopolysaccharide(LPS)-induced disseminated intravascular coagulation(DIC) in vivo and in vitro,and explore whether NF-κB signaling pathway is involved in ATL-Ⅰ treatment.Methods:New Zealand white rabbits were injected with LPS through marginal ear vein over a period of 6h at a rate of 600 μg/kg(10 mL/h).Similarly,in the treatment groups,1.0,2.0,or 5.0 mg/kg ATL-Ⅰ were given.Both survival rate and organ function were tested,including the level of alanine aminotransferase(ALT),blood urine nitrogen(BUN),and TNF-α were examined by ELISA.Also haemostatic and fibrinolytic parameters in serum were measured.RAW 264.7 macrophage cells were administered with control,LPS,LPS + ATL-Ⅰ and ATL-Ⅰ alone,and TNF-α,phosphorylation(P)-IκBα,phosphorylation(P)-NF-κB(P65) and NF-κB(P65) were determined by Western blot.Results:The administration of LPS resulted in 73.3%mortality rate,and the increase of serum TNF-α,BUN and ALT levels.When ATL-Ⅰ treatment significantly increased the survival rate of LPS-induced DIC model,also improved the function of blood coagulation.And protein analysis indicated that ATL-Ⅰ remarkably protected liver and renal as decreasing TNF-α expression.In vitro,ATL-Ⅰ obviously decreased LPS-induced TNF-αproduction and the expression of P-NF-κB(P65),with the decrease of P-IκBα.Conclusions:ATL-Ⅰ has protective effect on LPS-induced DIC,which can elevate the survival rate,reduce organ damage,improve the function of blood coagulation and suppress TNF-α expression by inhibiting the activation of NF-κB signaling pathway. Objective: To investigate whether atractylenolide I (ATL-I) has protective effect on lipopolysaccharide (LPS) -induced disseminated intravascular coagulation (DIC) in vivo and in vitro, and explore whether NF- [kappa] B signaling pathway is involved in ATL-I treatment. Methods: New Zealand white rabbits were injected with LPS through marginal ear vein over a period of 6 h at a rate of 600 μg / kg (10 mL / h). Similarly, in the treatment groups, 1.0, 2.0, or 5.0 mg / kg ATL-I were given.Both survival rate and organ function were tested, including the level of alanine aminotransferase (ALT), blood urine nitrogen (BUN), and TNF-α were examined by ELISA. Alfa haemostatic and fibrinolytic parameters in serum were measured .RAW 264.7 macrophage cells were administered with control, LPS, LPS + ATL-I and ATL-I alone and TNF-α, phosphorylation (P) -IκBα, phosphorylation (P) -NF-κB (P65) (P65) were determined by Western blot. Results: The administration of LPS resulted in 73.3% mortality rate, and the increase of s erum TNF-α, BUN and ALT levels. When ATL-I treatment significantly increased the survival rate of LPS-induced DIC model, also improved the function of blood coagulation. And protein protein analysis showed that ATL-I remarkably protected liver and renal as decreasing TNF-α expression in vitro, ATL-I obviously decreased LPS-induced TNF- α production and the expression of P-NF-κB (P65), with the decrease of P-IκBα. Conclusions: ATL-I has protective effect on LPS -induced DIC, which can elevate the survival rate, reduce organ damage, improve the function of blood coagulation and suppress TNF-α expression by inhibiting the activation of NF-κB signaling pathway.