The Effect And Plausible Mechanisms Of Valsartan On Atherosclerotic Plaque In Wistar Rat

Objective: To explore the effect of valsartan on atherosclerotic plaque.Methods:30wistar male rats were fed with high-cholesterol diet, andintraperitoneally injected of vitamin D36hundred thousand IU/kg at the beginning ofthe feeding, then the endothelium damage by balloon injury on the seventh day of thefeeding.30wistar male rats were divided into three groups:model group、low dosesof valsartan group、high doses of valsartan group, group A fed with water and theplacebo, group B fed with low concentration of valsartan20mg/kg/d on the day beforeballoon injury,group C fed with high concentration of valsartan40mg/kg/d on the daybefore balloon injury,12weeks later, all of the animals were killed,and blood wassampled from the hearts, MMP9、AngII of serum were dectected by ELISA. Theplaque pathologic morphology was observed by HE staining, Neointimal thickness,medial thickness, neointimal/medial thickness were measured by computer imageananysis technique. And the expression of MMP9and AngII in plaques were assayedwith Immunohistochemical staining.Results:1.HE staining shows that inflammatory cells of intima, and intimalthickening,foam cells and lipid content of intima accumulation in group A were moreseverer than group B and C;2.The level of neointimal thickness, neointimal/medial thickness in group A wassignificantly higher than group B and C（P＜0.05）, The level of medial thickness ingroup A was significantly lower than group B and C（P＜0.05）; The level ofneointimal thickness, neointimal/medial thickness in group B was significantlyhigher than group C（P＜0.05）. The level of medial thickness in group A and B isindiscrimination.3.The level of serum MMP-9and AngII in group A was significantly higher thangroup B and C（P＜0.01）,and group C was lower than group B（P＜0.01）;4.As show Immunohistochemical staining, the expression of significantly increased ingroup A than other groups（P＜0.01）and group C was lower than groupB（P＜0.01）; Conclusion:Valsartan may be inhibiting the development of plaques and stabilize vulnerableplaques by reducing level of AngII and bloking activity of AngII.