Elium leads to the increased permeability of endothelium and adhesiveness of leukocytes to artic wall. The production of procoagulant agents including vasoactive molecules, cytokines and growth factors can also be induced in endothelium. Blood monocytes adhere to epithelium, migrate into intima and become intimal macrophages, then change to foam cells by excessive ingestion of modified lipoprotein and gradually form the so called fatty streak [2]. The initial stage of inflammation of atherosclerosis is usually silent and long with increased adhesion of monocytes in arterial endothelium [4]. Adhesion molecules and monocyte chemotactic protein-1 (MCP-1) participate in the progress and play an important role. Fisrtly, selectin including E-selectin (E-sel), P-selectin(P-sel), and L-selectin (L-sel) facilitate the rolling of molecules on the surface of endothelium cells, then adhesion molecules, such as vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) mediate the advanced and firm adhesion of monocytes. Lastly, with the function of MCP-1, monocytes pass though endothelium and migrate into intima [5,6]. Damaged endothelial cells, arterial lesions from atherosclerosis experiment model and human all show increased expression of these molecules including E-sel, ICAM-1, VCAM-1 and MCP-1 [7,8]. Therefore, one possible mechanism for ameliorating atherosclerosis is the down-regulation of pro-atherogenic molecules such as E-sel, ICAM-1, VCAM-1 and MCP-1.Besides, in the inflammatory progress of atherosclerosis, activation of endothelial cells and mactophages leads to the release of various kinds of cytokines, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28499442 chemokines, and growth factors, which in return regulate the continued and advanced accumulation and migration of leukocytes, thus induce further inflammation [2]. Pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-) and interleukin-1beta (IL-1) participate in it by inducing E-sel, ICAM-1 and VCAM-1 expression in endothelial cells [9], releasing of other inflammatory mediators and inducing apoptosis of endothelial cells. Previous studies revealed that elevated levels of TNF- and IL-1 in patients with CVD have been detected [10,11], indicating that TNF- and IL-1 are two important cytokines in vascular inflammation and Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone web highly associated with atherosclerosis. Recent studies also suggested that, inflammatory biomarkers such as TNF-, IL1, E-sel, ICAM-1, VCAM-1 and MCP-1 may play a potential role for the prediction of risk for developing CVD and may correlate with the severity of CVD [12,13]. Kaempferol(3,5,7-trihydroxy-2-(4-hydroxyphenyl)-4H1-benzopyran-4-one), a yellow compound with a lowmolecular weight (MW: 286.2 g/mol), is a common natural flavonoid. This flavonoid is abundant in many plantderived foods and traditional medicine. It has been reported that kaempferol and its glycosides have many kinds of pharmacological activities, such as antioxidant, antiinflammatory, anticancer, antimicrobial, neuroprotective, antidiabetic, analgesic and anti-allergic activities [14]. And results of some studies suggested that the dietary intake of kaempferol-rich foods can reduce risk of developing several disorders including cardiovascular diseases [15,16]. Therefore we considered kaempferol to be a potent and effective agent against atherosclerosis. So far, the researches about the antioxidant, anti-inflammatory and cardioprotective effect of kaempferol have been mostly centered on endothelium cells in vitr.