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
机构地区:[1]新乡医学院第三附属医院,河南新乡453003 [2]新乡医学院药学院 [3]新乡医学院病理学教研室
出 处:《医药论坛杂志》2014年第5期1-3,6,共4页Journal of Medical Forum
基 金:河南省科技厅攻关科研基金资助(0524410058)
摘 要:目的观察家兔急性缺血再灌注后心肌组织中半胱氨酸蛋白酶-3(caspase-3)表达对心室功能影响。方法家兔30只,分对照组(10只),缺血组(10只),再灌注组(10只)。缺血组套扎左冠状动脉前降支30 min,再灌注组套扎30 min后再灌注120 min,对照组游离左冠状动脉前降支不结扎。超声心动图测量左室收缩功能,采用RT-PCR和免疫组化方法检测caspase-3基因与蛋白表达情况。结果对照组:各项指标基本正常。缺血组与对照组比较:caspase-3蛋白表达明显增高(P<0.01);caspase-3 mRNA表达显著增强;左室应变率明显降低(P<0.01)。再灌注组与缺血组比较:caspase-3蛋白表达进一步增高(P<0.01);caspase-3 mRNA表达也有所增强;左室应变率有所恢复,但仍明显低于对照组(P<0.05)。结论缺血再灌注激活capase-3是导致与心室功能的改变的重要原因。Objective To observe the affect of caspase - 3 expression at heart ventricular function following acute ischemia reperfusion in rabbits. Methods Thirty rabbits were divided into ischemia, reperfusion, and control groups. Left anterior descending coronary artery (LAD) were occluded 30 rain in ischemia group, reperfusion group were studied at LAD ligation 30 min, following reperfusion 120 rain ,with- out LAD ligation were used as control group. The left ventricular segmental function were detected by echocardiography using strain rate anlysis software. Caspase -3 mRNA and protein expression were analyzed by RT - PCR and immunohistochemistry. Results The peak strain rate ( SRpeak ) in ischemia group decreased obviously ( P 〈 0.01 ) , and postsystolic compression ( PSC ) was found in ischemia segment. SRpeak in- creased slightly after reperfusion 120 min, but still decreased than control group. Caspase -3 mRNA and protein expression increased more significantly in ischemia group than that in control group. And significantly increased in reperfusion group ( P 〈 0. 01 ). Conclusion Myocardial ischemia reperfusion activate Caspase - 3 expression may be was significance cause of induce the left ventricular function chang.
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:216.73.216.28