A Study On The Prevention And Cure Effect Of Benazepril On Rabbit Experimental Atherosclerosis Models

In recent years , the morbidity and mortality of coronary heart disease and cerebravascular disease induced by atherosclerosis have been graduolly increasing in China, presenting a great challenge for health professionals to look for an approch to delay, stabilize and reverse the development of atherosclerosis, and to find out an early treatment for this principle cause of deaths all over the world.The objective of our study is to investigate the effeet of Benazepril on the smooth muscle cell proliferation and migration at cellular and subcellular level, on theformation and development of atherosclerosis, and their relation to endothelin (ET), lipid peroxidation (LPO), nitric oxide (NO) , tumour necrosis factor (TNF), interleukin-6 (IL-6), with the measurement of blood lipid level, the microscopitc and electron microscopic pathology examination, so providing theoretical basis for of role Benazepril's in the prevetion and early treatment of atherosclerosis. Rabbits were randomly divided into three groups: the control group, the atherosclerosis group, andpretreatmenr(withSeleni -um+Vitamine E) group. The secondary objecteve is to find an improved method to develop rabbit model of atherosclerosisOur study showed that Benazepril andSelenium+Vitamine E could inhibif the increace of blood triglycerides and low density lipoprotein, especially when used as an pretreatment but there were no significant effect on the levels of blood high density lipoprotein and cholesteroids. The atherosclerosis lesion in the pretreatment group was sigificantly smaller than other groups. Microscopic and electron microscopic exami nation showed that Benazepril could inhibit smooth muscle cell protiferation and migration. The smooth muscle cells in pretreatment group were mainly contracted type. Benazepril could also increase the blood levels of NO, and reduce the levels of ET, LPO, TNF and IL-6.The rabbit model of atherosclerosis was successfully developed in our study, which has proved that Benazepril by regulating the levels of LDL and the balance of ET/NO, could inhibit the injury of endothilium cell, the initial event of atherosclerosis, and that Benazepril and Selenium +Vitamine E could inhibit the LPO, and delay the progress of atherosclerosis lesions from stable to active and then to rupture by inhibiting TNF. Our study also show that Benazepril could inhibit SMC proliferation and migration, which are the key processes of theathe- rosclerosis development, inhibit their transformation from contraeted type to synthesized type. Benazepril had a potential role in the prevention control and treatment of atherosclerosis, especially in the management of post-PTCA SMC proliferation and migration.