Objective To explore the possible mechanism of Wenban Decoction（ WBD） on the formation and rupture of unstable plaque of atherosclerosis（ AS）. Methods AS model was induced by high lipid diet in Apo E knockout mice. Sixty successfully modeled mice were equally randomized into 5 groups including control group（ CG）

western medicine group（ WMG）

and WBD groups（ WBDGs） consisting of low

middle and high dose groups. Twelve C57 BL /6J mice were also prepared as blank group（ BG）. During experiment

the BG received no intervention; CG took normal saline 0. 3 ml daily; low

middle and hight dose WBDGs were treated by WBD 6. 175

12. 35 and 24. 7 g / kg·d

respectively; WMG was administered avarstatin 27. 3 mg / kg·d. The treatment lasted for 13 weeks by gastric lavage. Then the mice were killed to reap abdominal aorta for HE stain. The mRNA levels of Tolllike receptors（ TLR4） of each group were assayed. Results Atherosclerotic plaque were observed in the aorta of CG mice with an overwhelming formation of foam cells and occasional filtration of inflammatory cells. The endarterium of mice from high and low dose WBDGs were smooth with occasional injury. The TLR4 mRNA expressions of CG were higher than BG（ P < 0. 01）; The expressions of low

middle and high dose WBDGs and WMG were lower than MG（ P < 0. 01）. Low and middle dose WBDG showed the expressions of TLR4 significantly higher than WG（ P <0. 01）. No statistical significant difference was observed between the expressions of high dose WBDG and WMG（ P >0. 05）. Conclusion Inhibiting the expression of TLR4 in abdominal aorta tissue might be one of the possible mechanisms for WBD to prevent from the formation and rupture of AS plaque..