Investigation Of The Effect Of Insulin On ICAM-1, VCAM-1 In Endothelial Cell

Background:Artherosclerosis (AS) is a common and frequently disease which is associated with a significant morbidity and mortality. Coronary heart disease (CHD) is one of the main causes of premature death in industrialized countries, and its prevalence has been increasing in developing ones. Recent studies provide evidence that an inflammatory reaction is an essential component in the appearance and development of the atherosclerotic lesion. inflammatory cells roll along and adhere to blood vessel endothelium, and meanwhile penetrate through endotheliocyte while releasing various active cell material that causes proliferation of vascular smooth muscle cells, forming foam cell, and finally leading to AS. ICAM-1 and VCAM-1 both belong to Cellular adhesion molecules (CAMs), investigation shows that ICAM-1 and VCAM-1 play an important role in cardiovascular disease. Insulin has recently emerged as a significant vascular hormone with important links to the pathophysiology of atherosclerotic vascular disease. Vascular endothelium is the main organ under the influence of INS, and INS plays an important part in maintaining the normal function of blood vessel endothelium. It is proved by experiment that internal hyperinsulinemia causes the externalization disproportion of vascular endothelial cell ET-1 and NO, promotes the occurrence and development of DM blood vessel complication, and becomes the main factor of AS. Does hyperinsulinemia correlate with endotheliocyte adhesion molecule during the formation and growth of AS? This article will focus on animal model and molecular level, and tries to provide a new theoretical base for exploring the function of hyperinsulinemia in AS.Objective:1. To observe the influence of hyperinsulinemia on the expression of VEC VCAM-1 and ICAM-1 in the experiment;2. To observe the influence of INS on the expression of human VEC VCAM-1 and ICAM-1.