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作 者:艾文[1] 谢培益[1] 陈延伟[1] 方红城[1] 陈菲[1] 吴保泉[1] 刘宗波[1] 苏又苏[1]
机构地区:[1]广东医学院附属南山医院心内科,广东深圳518052
出 处:《心血管康复医学杂志》2013年第3期219-222,F0003,共5页Chinese Journal of Cardiovascular Rehabilitation Medicine
基 金:深圳市科技计划资助项目(201103317)
摘 要:目的:观察表皮生长因子受体(EGFR)在大鼠糖尿病性心肌病(DCM)纤维化中的作用。方法:将雄性Wistar大鼠25只随机分为正常对照组(n=10)和DCM组(建立的DCM大鼠模型,n=15),比较两组各指标的差异显著性。结果:造模2周后开始,与正常对照组相比,DCM组体重显著降低(P<0.05),空腹血糖水平明显升高(P<0.01);8周时超声心动图显示,与正常对照组相比,DCM组左室收缩末期内径(LVESd)[(3.23±0.19)mm比(3.65±0.26)mm]明显增加,左室舒张末期内径(LVEDd)[(7.07±0.43)mm比(6.21±0.25)mm]明显减小,左室射血分数(LVEF)值[(82.71±2.18)%比(72.5±3.02)%]明显降低(P均<0.05)。HE染色可见心肌细胞增生肥大、排列紊乱;Masson染色可见心肌纤维细胞增生明显,心肌胶原容积分数显著增大;Western blot方法检测EGFR表达水平显著高于正常对照组[光密度值(4.18±0.54)比(1.53±0.12)],P均<0.01。结论:表皮生长因子受体可加速糖尿病性心肌病大鼠心肌纤维化。Objective:To observe role of epidermal growth factor receptor(EGFR)on fibrosis in rats with type 1diabetic cardiomyopathy(DCM).Methods:A total of 25male Wistar rats were randomly divided into normal control group(n=10)and DCM group(established DCM model,n=15).Results:Since two weeks after modeling,compared with normal control group,there was significant decrease in body weight(P〈0.05)and significant elevated in FBG level(P〈0.01)in DCM group;Ultrasonic cardiogram(UCG)of 8th week indicated that compared with normal control group,there was significant increase in left ventricular end-systolic dimension(LVESd)[(3.23± 0.19)mm vs.(3.65±0.26)mm],and significant decrease in(left ventricular end-diastolic dimension)LVEDd [(7.07±0.43)mm vs.(6.21±0.25)mm]and left ventricular ejection fraction(LVEF)[(82.71±2.18)% vs.(72.5±3.02)%]in DCM group,P〈0.05all.In DCM group,HE staining indicated that myocardial cells were hypertrophic and disorganized;Masson staining indicated that there was significant myocardial fibrocyte proliferation and myocardial collagen volume fraction significantly increased;Western blot method detection indicated that expression level of EGFR was significantly higher than that of normal control group[optical density(4.18±0.54) vs.(1.53±0.12)],P〈0.01all.Conclusion:Epidermal growth factor receptor can accelerate myocardial fibrosis in rats with diabetic cardiomyopathy.
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