| Objective To verify the clinical therapeutic effect of Chinese herbal prescription fordispeling blood stasis in preventing Atherosclerosis, meanwhile, to investigate itsfunctions in preventing atherogenesis through animal experiments.Methods Open randomized control trial was employed in clinic and simvastain wastaken as control medicine. The therapeutic difference between prescription fordispeling blood stasis and simvastatin in patient's symptom, blood-lipid, bloodrheology and other index were observed. In animal experiments, SD rats were inducedinto atherogenesis through hyperlipid food to study the effects of prescription fordispeling blood stasis in regulating lipid, protecting endothelial functions throughhistochenical stain and imunosorbent assay methods,thereby, to preliminarilyinvestigate the ways of prescription for dispeling blood stasis in preventingatherogenesis.Results The total effective rate were 90% and 53.33% in treating atherosclerosis byprescription for dispeling blood stasis and simvastain respectively, and prescription fordispeling blood stasis had the functions in reducing TC,TG. Prescription for dispelingblood stasis was better than simvastatin in deceasing whole blood and plasmaviscosity, and improving patient's symptoms. Prescription for dispeling blood stasishad the functions in boosting up PPARγ's expression. Through animal experiments, itwas proved that Prescription for dispeling blood stasis could effectively regulateblood-lipid, and this prescription had the actions in enhancing NO level, inhibitingICAM-1,VCAM-1 expression in vascular wall and improving lipoidal structure oferythrocytic cytomembrane.Conclusion The therapeutic effects of prescription for dispeling blood stasis intreating atherosclerosis were certain and it was better than simvastain in improvingpatient's symptoms. Prevention of atherogenesis by prescription for dispeling bloodstasis may be involved in the following ways. (1)Through regulating lipid level toincrease HDL, to reduce LDL and decrease lipoid sedimentation under vascularendothelial cells. (2)Reducing the level of fibrinogen, regulating high plasma viscosityof blood, decreasing sediment of lipide. (3)Regulating blood vessel active substance,enhancing proportion of spreading blood vessel substance. (4)Through inhibitingICAM—1and VCAM—1 expression to decrease intercellular adhesion betweenendothelial cells and other cells. (5)Through adjusting expression of PPARγgene toreduce cell's conglomeration. (6)Protecting endothelial functions and protectingendothelial structure to decrease damage of lipoid on endothelia. |