At the same time, the serum high-density lipoprotein-cholesterol (HDL-C) was slightly lower in LPS/fat mice than non LPS/fat mice. However, the productions of TC and TG in the BV treated mice were conversely decreased compared to mice with atherosclerotic lesions. Furthermore, BV treatment longer than 8 weeks boosted HDL-C concentration compared with other groups. LPS and atherosclerotic diet induced a significant expression of tumor necrosis factor (TNF)-ÃŽ± and interleukin (IL)-1ÃŽÂ² from the serum compared with the normal control (p < 0.05). The contents of cytokines reduced consistently in the BV treatment groups compared with those in LPS/fat group. BV significantly reduced ICAM-1, VCAM-1, transforming growth factor-ÃŽÂ²1 (TGF-ÃŽÂ²1) and fibronectin in aorta compared with LPS/fat treated animals (p < 0.05). A similar pattern was also observed in the heart. The reduction of TGF-ÃŽÂ²1 and fibronectin gene levels induced by BV was striking. The alleviating effect of BV on atherosclerotic changes in the artery and heart was further supported by histopathological and immunohistochemical approaches. In conclusion, BV has antiatherogenic property via its lipid-lowering and anti-inflammatory mechanisms.It is well recognized that vascular inflammation is involved in the pathogenesis of atherosclerosis. Infiltration of circulating leukocytes into the inflamed vascular endothelium requires the up-regulation of adhesion molecules of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). The components of bee venom (BV) used in the current study were carefully scrutinized with chromatography. Despite of its well known anti-inflammatory properties, there are no reports regarding the influence of BV on the expression of cellular adhesion molecules to vascular endothelium. Much information does exist about the effect of atherogenic diet on atherosclerotic changes in the artery. However little is known about how BV affects the molecular mechanisms and the levels of gene expression involved in the anti-inflammatory process. Experimental atherosclerosis was induced by lipopolysaccharide (LPS) injection to mice maintained on an atherogenic diet. Animals were divided into 3 groups: (a) control group; (b) a LPS/fat group maintained on an atherogenic diet along with intraperitoneal injections of LPS; (c) a LPS/fat + BV group that was maintained on an atherogenic diet, and given LPS and intraperitoneal BV injections. At the end of each treatment period, serum levels of total cholesterol (TC) and triglyceride (TG) were significantly higher in LPS/fat mice than in the control mice (p < 0.05).