检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:杨冰[1] 廉瑞青[1] 李若凡[1] 刘伟[1] 唐红梅[1] 王艳梅[1] 张晓东[2]
机构地区:[1]北京协和医学院基础学院中国医学科学院基础医学研究所人体解剖与组织胚胎学系,北京100005 [2]清华大学医学院,北京100084
出 处:《中国临床解剖学杂志》2008年第2期175-178,共4页Chinese Journal of Clinical Anatomy
基 金:清华大学裕元基金(20240000546)
摘 要:目的:观察曲尼司特对大鼠心肌梗塞(MI)后左室心肌纤维化(MF)和转化生长因子-β1(TGF-β1)表达的影响。方法:结扎左冠状动脉前降支建立大鼠心肌梗塞模型,随机分成3组:假手术组、MI模型组和曲尼司特治疗组(400 mg.kg-1.d-1)。4周后测定血流动力学指标评价心功能,测量左心室重与体重之比、梗死面积、非梗死区心肌羟脯氨酸(HYP)含量和TGF-β1的表达。结果:与MI模型组比较,曲尼司特治疗后心肌梗死面积无明显改变(P>0.05),但左室功能显著改善(P<0.05),左心室肥大减轻(P<0.01),非梗死区心肌HYP含量和TGF-β1表达降低(P<0.05)。结论:曲尼司特可下调大鼠非梗死区心肌TGF-β1表达及降低HYP含量,减轻MI后左室非梗死区心肌纤维化,改善心功能。Objective: To observe the effects of tranilast on myocardial fibrosis (MF) and expression of transforming growth factor-β1 (TGF-β1) in the non-infarcted myocardium after myocardial infarction (MI) in rots. Methods: MI model was established in male Wister rots by ligation of left anterior descending coronary artery. The rots were randomly divided into three groups: sham-operated group, MI model group and tranilast treatment group (400 mg·kg^-1·d^-1). After 4 weeks of treatment, the cardiac function was assessed by hemodynamic measurements, the ratio of left ventricular weight and body weight, infarct size, hydroxyproline (HYP) content and expression of TGF-β1 were measured, Results: Compared with MI model group, tranilast did not decrease infarct size(P〉0.05 ), but it did improved left ventricular function (P〈0.05), and decreased the left ventricular hypertrophy (P〈0.01), the HYP content and TGF-β1 expression of non-infarcted myocardium (P〈0.05). Conclusions: Tranilast can inhibit myocardial fibrosis through decreasing the expression of TGF-β1 which is showed to play an important role in MF, and improve left ventricular function after MI in rats.
关 键 词:心肌梗塞 心肌纤维化 曲尼司特 转化生长因子-Β1
分 类 号:R542.2[医药卫生—心血管疾病]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.3