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Rosuvastatin Improves Endothelial Function By Increasing Enos Mrna Expression

Posted on:2010-05-02Degree:MasterType:Thesis
Country:ChinaCandidate:Y LiangFull Text:PDF
GTID:2194360302976298Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Background:Coronary atherosclerotic heart disease refers to coronary scleratheroma cause lumens stenosis and occlusion,heart disease because of myocardial ischemia necrosis and coronary artery functionality revised such as coronary artery spasm,collectively called coronary heart disease,the mechanism of coronary heart disease supported by most hakeem is atherosclerotic injuries and reaction theory.The theory presumes atherogenic risk factor all injures artery endothelium in final.Now the patient of coronary heart disease is widespread used statins as a medicine of adjusting lipoid,statins draw assistance from inhibiting reducase in the way of cholesterol metabolism,affect cholesterol metabolism.Nowadays the research presume statins used in acute stage can precipitate endothelium release nitric oxide (NO),have the same effect of nitrate,and have the effect of anti-inflammatory and stabilizing plaque in long-term.It can also decrease the death rate of coronary heart disease and incidence of myocardial infarction.Statins can be classified into lipophilic HMG-CoA reductase inhibitors(atorvastatin,simvastatin,cervastatin,fluvastatin,and lovastatin) and hydrophilic HMG-CoA reductase inhibitors(pravastatin and rosuvastatin).Rosuvastatin is a kind of hydrophilic statins,can display greatest uptake into hepatocytes compared with other cells.Endothelial nitric oxide synthase(eNOS) is a calcium-dependent enzyme and forms NO in endothelial cells under physiological conditions.NO then diffuses into adjacent smooth muscle cells,activating guanyl cyclase,producing cyclic guanosine 5' monophosphate that mediates vascular relaxation via protein kinase G.Vascular inflammation and endothelial dysfunction in disease states are associated with a loss of eNOS-produced NO because of the vital role of this cascade in maintaining a non-thrombogenic endothelial cell surface.Now the research prompt statins may affect the activity of eNOS or the gene expression of eNOS.This study wants to investigate the effect of statins on endothelial function in the coronary heart disease patient.Objective:To investigate the effects of statin on endothelial function and the level of eNOS mRNA expression.Methods:30 CHD patients diagnosed by coronary angiography were divided into 2 groups:the group one(G1,n=20)and group two(G2,n=10) 20 patient with angiographically normal coronary arteries was servered as control group(G3,n=20). Both G1 and G3 were given Rosuvastatin for 4 weeks.Endothelial dependent flow-mediated vasodilatation(FMD) and the levels of eNOS mRNA expression were detected by high-resolution ultrasound and RT-PCR to assess the endothelial function before and after 4 weeks' treatment.Data were analyzed with SPSS 10.0.Continuous variables are described as means±SD((?)±s) and were compared by independent-Sample T Test.P<0.05 was considered statistically significant.Results:①The level of eNOS mRNA expression and FMD in G1 and G2 had no statistical difference before the study.②The level of eNOS mRNA expression in G1 was increased and FMD was improved 4 weeks later(P<0.05).The level of serum total cholesterol and LDL cholesterol in both G1 and G3 showed a decrease after 4 weeks' treatment(P<0.05). ③The level of eNOS mRNA expression and FMD in G2 had no statistically significant after 4 weeks'treatment.④In G1 and G3 the level of eNOS mRNA expression was increased and FMD was improved after treatment(P<0.05).Conclusions:Rosuvastatin could improve endothelial function by increasing the level of eNOS mRNA expression.
Keywords/Search Tags:Rosuvastatin, Coronary artery disease, Endothelial nitric oxide synthase, Endothelial function
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