Expression of plasma bone morphogenetic protein-4 in patients with coronary heart disease and intervention effect of rosuvastatin
10.3760/cma.j.issn.1008-6315.2014.05.013
- VernacularTitle:冠心病患者血浆骨形态发生蛋白4表达及瑞舒伐他汀的干预作用
- Author:
Lijian PAN
;
Juanjuan PAN
;
Lei LIU
;
Yijun SHI
;
Hui GONG
- Publication Type:Journal Article
- Keywords:
Coronary heart disease;
Bone morphogenetic protein-4;
Rosuvastatin;
Oxidative stress;
Endothelial function
- From:
Clinical Medicine of China
2014;30(5):489-492
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes of plasma bone morphogenetic protein-4 (BMP-4) levels in patients with coronary heart disease (CHD) and rosuvastatin intervention effect on BMP-4 level.Methods Fifty-two patients with CHD and 35 health people were enrolled in this study as CHD group and control group.ELISA method was used to detect the concentration of plasma BMP-4.Analyzed the relationship between plasma BMP-4 and blood lipids,flow-mediated dilation (FMD),nitric oxide (NO),cyclooxygenase-2 (COX-2),malondialdehyde (MDA) and superoxide dismutase (SOD).And observed the changing of plasma BMP-4 before and after rosuvastatin intervention.Results Plasma BMP-4 level in CHD patients was (7.53 ± 1.20) μg/L,higher than that of control group ((3.81 ± 0.79) μ g/L,t =3.541,P =0.006).After rosuvastatin treatment,plasma BMP-4 level in CHD patient was decreased from (7.53 ± 1.20) μg/L to (5.40± 0.98) μg/L (t =1.436,P =0.001).Plasma BMP-4 level was positively correlated with COX-2,MDA,low-density lipoprotein cholesterol,total cholesterol (r =0.395,0.350,0.274,0.288 respectively,P ＜ 0.01 or P ＜0.05).But,it was negatively correlated with NO,high-density lipoprotein cholesterol,SOD,FMD (r =-0.291,-0.253,-0.476,-0.320 respectively,P ＜0.01 or P ＜0.05).COX-2,SOD and FMD were independent risk factors of plasma BMP-4 in patients with CHD.Conclusion Oxidative stress and endothelial dysfunction are in patients with CHD.Rosuvastatin treatment can remarkably reduce plasma BMP-4 level,alleviate vascular endothelium injury induced by oxidative stress and improve endothelial function in patients with CHD.
