The Change Of The Quantity Of The Endothelial Progenitor Cells From Peripheral Blood And The Expression Of ENOS In Atherosclerotic Rats

BackgroundAtherosclerosis is the common and most important one in atherosclerotic vascular diseases, and is the most important pathological basis to generate many diseases, such as myocardial infarction, stroke, and other cardiovascular diseases. The incidence is increasing every year and is a serious threat to human health. Endothelial progenitor cells is the precursor cells of the vascular endothelial cells, it is the initial link of the atherosclerosis when vascular endothelial cells are injured and dysfunctional. Endothelial nitric oxide synthase is the enzyme which can determine the production of the nitric oxide, many studies have shown that, if the producton of nitric oxide which generated by eNOS was reduced, the result would lead to dysfunction of the endothelial cells, and eventually give rise to the generation of atherosclerosis. Thus, EPCs and eNOS may be involved in the occurrence and development of atherosclerosis and have become a hot topic of current researchs.The most basic pathologic feature is that from arterial intimal injury, after that,the general performance is that its function disorder, exposure the subinitimal tissue, that can increase the endothelial permeability to the lipoproteins and plasma components, then the endothelial function of balanced adjustment is declined, the synthesis and secretion of nitric oxide by endothelium is reduced, but the endothelin and the expression of endothelial adhering molecules are increased, then anti-thrombotic function of endothelium is disordered, after lipid aggregation, bleeding, thrombosis, and so on, then appeared that macrophage swallowed the lipid foam cells, extracellular lipid fused, formed the lipid core, unstable plaques(thin fibrous cap), stable plaque(under thin fibrous cap), then plaque ruptured and bleeding, the thrombosis of vascular in order, which make arterial initimal become thick, then the vascular wall become thick and hard, and then, the vascular wall loses its elasticity and the lumen become narrow, that lead to atherosclerosis.Endothelial progenitor cells have the effect of migratory, self-renewal and proliferation, play an important role in the course of proliferation and repair of the injurded endothelial cells, can be directed to differentiate into endothelial cells, and repair injured endothelial cells, and that the balance of damage and repair of the endothelium palys an important role in reducing atherosclerosis. Nitric oxide synthase is widely distributed in the body, in which eNOS is the most important. In vascular endothelial cells, nitric oxide which induced by eNOS has important physiological effects, such as can regulate blood pressure, maintain vascular tone, inhibit platelet aggregation and adhesion, inhibits smooth muscle cell migration and proliferation, regulate myocardial contraction and relaxant, and so on.However, the occurrence and development of the pathophysiology of the atherosclerosis has not yet been fully elucidated. A large number of studies have shown that atherosclerosis is not only an inflammatory disease, but also is a result of the together effect of the muti-gene and multiple environments factors. In the present studies, the study of mechanism between atherosclerosis and EPCs is relatively little, and between atherosclerosis and eNOS is less.ObjectionTo analyses the change of the quantity of the endothelial progenitor cells(EPCs) from peripheral blood and the expression of endothelial nitric oxide synthase(eNOS) in atherosclerotic rats. MethodsRats were divided into2groups:rats in group1(n=20) were fed with normal diet, group2(n=20) were sham-operated and fed with high-fat diet,group3(n=30) were treated with the endothelium of the arteries were injured by balloon followed by high-fat diet. Peripheral blood samples were drawn to isolate and culture EPCs respectively, EPCs populations were assessed using the colony forming unit assay (EPC-CFU) through an inverted phase contrast microscope after14days culture, and genetic content of eNOS was detected using the way of Real-time PCR90days later.Results1. Compared with G1, the number of endothelial progenitor cells in G2had no significant change (P＞0.05), but in G3was lower (P<0.01). Compared with G2, the number of endothelial progenitor cells in G3had significantly reduction (P＜0.01).2. Compared with G1, the expression of endothelial nitric oxide synthase in G2had no significant difference (P＞0.05), but in G3had less expression (P<0.01). Compared with G2, the expression of endothelial nitric oxide synthase in G3had significantly downregulation.(P＜0.01).ConclusionsCompared with G1and G2, the number of endothelial progenitor cells in G3had significantly reduction, and the expression of endothelial nitric oxide in G3had significantly downregulation, suggesting that there is endothelial dysfunction in atherosclerosis and the two may be involved in the atherosclerotic plaque occurance and development.