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目的观察心肌梗死局部转染整合素连接激酶(ILK)基因对大鼠心肌细胞凋亡以及心功能的影响。方法采用左冠状动脉前降支结扎法建立大鼠心肌梗死模型,并随机在梗死周围区注射ILK重组腺病毒(实验组,n=18)和空载病毒(对照组,n=17),4周后行经胸壁超声心动图检测其左室收缩末期容积(LVESD)、左室舒张末期容积(LVEDD)、室壁厚度及左室收缩比率(FS%);并分别使用原位末端转移酶介导标记(TUNEL)法及活化半胱天冬酶3(caspase-3)蛋白法检测大鼠心肌细胞的凋亡情况。结果与对照组比较,实验组心脏左室内径缩小[LVEDD:(6.9±0.8)比(7.8±1.1)mm;LVESD:(3.8±0.8)比(4.6±0.8)mm,均P<0.05]、心脏收缩功能改善[FS%:(46.0±5.7)比(40.9±5.8),P<0.05],心肌细胞凋亡率在大鼠心肌梗死周围区[(0.187±0.033)比(0.361±0.084)%,P<0.05]和梗死远区[(0.105±0.037)和(0.243±0.044)%,P<0.05]均显著下降。活化caspase-3的测定证明实验组大鼠较对照组大鼠心肌细胞凋亡显著减少。结论心肌梗死局部ILK基因过表达能抑制心肌梗死后大鼠左室重构,改善其心功能。
Objective To investigate the effect of local transfection of ILK gene on cardiomyocyte apoptosis and cardiac function in rats with myocardial infarction. Methods The left anterior descending coronary artery ligation was used to establish a model of myocardial infarction in rats. Randomly injected ILK recombinant adenovirus (experimental group, n = 18) and empty vector (control group, n = 17) Left ventricular end-systolic volume (LVESD), left ventricular end-diastolic volume (LVEDD), wall thickness and left ventricular systolic ratio (FS%) were measured by thoracic echocardiography. The apoptosis of rat cardiomyocytes was detected by TUNEL assay and caspase-3 protein assay. Results Compared with the control group, the left ventricular diameter (LVEDD: (6.9 ± 0.8) vs (7.8 ± 1.1) mm; LVESD: (3.8 ± 0.8) vs (4.6 ± 0.8) mm, P <0.05] (0.187 ± 0.033) vs (0.361 ± 0.084)% in the peripheral area of myocardial infarction (P <0.05) , P <0.05] and distal infarction [(0.105 ± 0.037) and (0.243 ± 0.044)%, P <0.05]. Activation of caspase-3 assay showed that the experimental group rats compared with the control group, myocardial apoptosis significantly reduced. Conclusion Overexpression of local ILK gene in myocardial infarction can inhibit left ventricular remodeling and improve cardiac function in rats with myocardial infarction.