Effects Of Simvastatin On Number And Adhesiveness Of Endothelial Progenitor Cells Cultured In Vitro From Umbilical Vein Blood

As a first-line drug for the prevention and treatment of coronary heart diseases, HMG-CoA reductase inhibitors -statins on lipid-lowering Cholesterol drugs have been confirmed with a number of cardiovascular protection, including the improvement of endothelial function, inhibiting of smooth muscle cell proliferation and migration ,the inhibition of platelet aggregation, and the inflammatory response of microvascular. Some recent studies have showed that statins also promote angiogenesis after acute ischemic , accelerate endothelialization of vascular injury induced by Balloon and reduce neointimal thickening,but the two roles are closely related with the EPCs.EPCs have characteristics of self-proliferation , homing directionally and can be directed to differentiate into mature endothelial cells. Prospects of clinical application are broad. Recent studies have provided a favorable evidence that neovascularization after the birth don't only rely on preexisting vascular sprouting, but also on the EPCs from bone marrow and circulating blood . Only if endothelial integrity ,vascular normal function structure can keep. PTCA make intima damaged ,leading to neointimal thickening .As stent lesions and vascular endothelial vasodilator injury vascular elastic fibers in the damaged layer extends to the arterial intima. Vascular injury led to the injuried site migration of vascular smoothmuscle cell proliferation and the formation of the thrombus thus leading to the stent restenosis (In-stent restenosis). Neointimal VSMC activation after injury in half an hour you can see from contraction to a synthetic, thus triggering the proliferation of VSMC migration and matrix synthesis. Near the site of injury vascular endothelial cells (ECs) expand rapidly, move to the injury, vascular injury coverage endometrium. Once the damage was VEC coverage of the endometrium, the reaction of endometrial thickening will stop. Therefore, the promotion of renewable endothelial cell injury site so as to restore the integrity of the endometrium. Prevention on restenosis has become one of the key measures after percutaneous transluminal coronary angioplasty and stent. Volume and quality of EPCs from the circulating blood are and closely related to repair endometrial.Objective : Isolate, Purificate, cultured EPCs from human umbilical vein blood. Observe the effects on expand and adhesion ability of EPCs in different concentrations of simvastatinMethods : (1)EPCs were isolated by density gradient centrifugation in human umbilical vein .(2). Immunofluorescence assay endothelial cell uptake and absorption DiL-acLDL. EPCs quantitative detection of surface markers by flow cytometry : CD133, CD34 antigen expression and KDR. (3) EPCs inverted microscope observation of the morphological changes, cell count and the growthcurve. (4), Simvastatin pm : 0, 0.01, 0.1, 1 and 10μmol/ L. EPCs proliferation observed by MTT, adhesion evaluation of the level of EPCs by counting the number of adherent cellResults (1) a long fusiform cells, the cells were smaller particles spindle shape ;6-10d adherent cell growth for the spindle cell latency and increased the number of proliferating; 375mg colony-like growth into cell fusion, the cells were significantly increased access to growth platform. (2), fluorescence microscopy revealed absorption DiL-acLDL. uptake in the cells were red, green fluorescence, two fluorescent yellow-dyed hair; Results : CD133 expression detected by flow cytometry, and KDR CD34 antigen were : (3%). (3), MTT colorimetric results showed that simvastatin EPCs proliferation activity, a few strong adherent of EPCs. However, the concentration of 1μL EPCs proliferation of the most dynamic. 24 h, 48 h and which role, the same group not obvious difference in the number of adherent cellsConclution:(1), we can isolate, purify, amplificate and culture EPCs from human umbilical vein. EPCs experience in vitro culture conditions growth platform. The content of normal body EPCs limited and can not meet the actual needs of the experimental and clinical application. EPCs in vitro proliferation significantly IN environment of endothelial growth using cultured EPCs to find a best time of the research and application. (2). HMG-CoA reductaseinhibitors can significantly increase the number and adhesiveness of EPCs .Innovation:(1),there are a variety of sources of EPCs, but the umbilical cord blood in the domestic reporting is less.(2),In addition to seeking a new role independence of lipid-lowering Cholesterol for the HMG-CoA reductase inhibitor .