| Atherosclerosis (AS) is a polygenic and multifactorial life-threatening disease induced by the interaction between environmental and hereditary factors. The pathogenesis of AS involves endothelial injury or dysfunction, attachment of monocytes to the endothelial cells; migration of the cells into the intima and their transformation into macrophages there, smooth muscle cells (SMC) migration from the media into the intima, proliferation of SMC, deposition of lipids, macrophage-foam cells generation and accumulation of extracellular matrix. In the developed countries, AS is NO.l human killer; in the developing countries, the morbidity and mortality caused by the heart and brain angiopathy as a result of AS is increasing, so how to cure AS is becoming a global concern.Intercellular adhesion molecule-I (ICAM-1, CD54) is one of the adhesion molecules, it is expressed on the surface of leukocytes and some nonhematopoietic cells, including vascular endothelial cells, vascular smooth muscle cells (SMC) and epithelial cells. The expression of ICAM-1 on endothelial cells is critical for the recruitment of leucocytes from the circulating blood into the early atherosclerotic lesions, while the expression of ICAM-1 on SMC results in increased adhesion of leucocytes to SMC and contributes to SMC migration and proliferation. So it is important to seek the effective medicine to inhibit the expressing of ICAM-1 for the prevention and treatment of AS.At present, although there are many ways to treat AS, most of them are not ideal. Western medicine is of single effect with harmful side effects. The interpretation of "blood stasis" and "stuffiness" in traditional Chinese medicine (TCM) is close to the meaning of "thrombosis", "the formation of atherosclerosis plaque " in modern medicine. The TCM for activating bloodand removing stasis such as coronary heart No. II (CH-II) and Salvia Injection (SI) have acquired positive effect and attracted universal attention. In the past, more attention was paid to the medicines' effect on reducing serum lipid, anti-coagulating, inhibiting SMC proliferation and migration, whereas, research on the adhesion molecule was somehow ignored. In this paper, we studied the new effects and mechanisms of AS treatment with TCM (CH-II and SI) for activating blood and removing stasis. 1. Establishment of rat AS model and assay of lipid, Ca2+, TNF- a , TXA2/PGI2 and NO in bloodThe model was established by feeding with fat-rich diet and high dose of vitaminDv Pathological changes and concentrations of lipid, Ca2+, TNF-a ,TXA2/PGl2 and NO in blood were measured.(1) Compared with intact layers of aorta without foam cells and calcification in normal rats, lesions in AS rats contained proliferative SMC, thickened intima which projected into lumen at some sites of aorta, calcification and foam cell-rich regions. All of these indicated that the rat AS model has been established successfully.(2) Levels of triglyceride (TG), total cholesterol (TC) and Ca2+ in serum were significantly higher in the AS rats than those in normal rats (p<0.05, p<0.01 , p<0.05 respectively).(3) Concentration of TNF- a in serum of AS rats (3.62 + 0.57 ng/mL) was significantly higher than that in normal rats (1 .83+0.24 ng/mL) (p<0.01 ).(4) Level of PGI2 in plasma of AS rats was significantly lower than that in normal rats (p<0.05), however, level of TXA2 showed no difference between two groups. The ratio of T/K. of AS rats (6.72 + 2.64) was significantly higher than that in normal rats (3.86+1 .42) (p<0.05).(5) Concentration of NCV in serum of AS rats (27.78+11.45 umol/L) was significantly lower than that in normal rats (52.41 + 10.27 umo/L)The results showed that high level of lipid, SMC proliferation and migration might impede the flow of blood and contribute to " blood stasis".TNF- a is one of cytokines involved in the AS formation. It can be secreted from monocytes, endothelial cells and SMC. So, the level of TNF- a in serum of AS rats was significantly higher than that in normal rats.
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