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背景整合素相关激酶(ILK)是心肌机械牵拉的一种感受器,对心肌收缩起调节作用。目的探讨心肌局部转染ILK基因对心肌梗死后大鼠的心功能的影响。方法大鼠冠状动脉左前降支结扎制成急性心肌梗死模型,在梗死周围区分别注射表达ILK的腺病毒载体(治疗组,n=8)或者不表达ILK的腺病毒载体(对照组,n=8)。免疫蛋白印迹法测定注射病毒载体后的心肌组织ILK的表达水平。术后4周,心导管法测定大鼠心功能。HE染色和免疫组化染色了解新生血管密度,心脏胶原含量等心肌组织形态变化。结果注射病毒载体后心肌ILK表达水平在2周左右达到顶峰,在4周左右逐渐减低。治疗组大鼠左室压力上升最大速度(+dp/dtmax)[(4930.1±1074.8)mmHg/s]较对照组明显增加[(3325.2±775.9)mmHg/s,P<0.01];治疗组的梗死边缘带的血管密度[(107.6±13.2)/高倍镜视野]较对照组明显增加[(69.0±11.0)/高倍镜视野,P<0.01];治疗组的梗死边缘带组织胶原含量[(27.2±6.3)%]较对照组明显降低[(35.1±9.1)%,P<0.01];治疗组的梗死边缘带的心肌细胞的密度[(320.5±61.6)/高倍镜视野]明显高于对照组[(280.9±58.9)/高倍镜视野,P<0.01],而治疗组的梗死边缘带的心肌细胞横径[(17.5±2.9)μm]要低于对照组[(24.1±3.6)μm,P<0.01]。结论梗死局部心肌的ILK局部注射,加强基因表达,可以改善梗死后大鼠的心功能,这可能和改善梗死周围区的血管生成和胶原含量,从而减轻组织缺血有关。
Background: Integrin-related kinase (ILK) is a type of sensor of mechanical pull of myocardium and regulates myocardial contractility. Objective To investigate the effect of myocardial transfection of ILK gene on cardiac function in rats after myocardial infarction. Methods Acute myocardial infarction (AMI) model was established by ligation of left anterior descending coronary artery in rats. Adenovirus vector expressing ILK (n = 8 in treatment group) or adenovirus vector without ILK injection (control group, n = 8). The level of ILK in myocardial tissue after injection of viral vector was detected by Western blotting. At 4 weeks after operation, cardiac function was measured by cardiac catheterization. HE staining and immunohistochemical staining to understand the changes of myocardial tissue such as neovascular density and cardiac collagen content. Results The expression level of ILK in myocardium reached the peak at 2 weeks after injection of virus vector and gradually decreased at 4 weeks. Compared with the control group, the maximal velocity of left ventricular pressure increase (+ dp / dtmax) in the treatment group was significantly higher than that in the control group [(3325.2 ± 775.9) mmHg / s, P <0.01] (107.6 ± 13.2) / high magnification field] (69.0 ± 11.0) / high magnification field (P <0.01). The content of collagen in the marginal zone in the treatment group was significantly higher than that in the control group [(27.2 ± 6.35%] was significantly lower than that of the control group [(35.1 ± 9.1)%, P <0.01]. The density of myocardial cells in the infarcted zone in the treatment group was significantly higher than that in the control group [(320.5 ± 61.6) / (280.9 ± 58.9) / high magnification (P <0.01). However, the diameter of myocardial cells in the infarct zone in the treatment group was significantly lower than that in the control group [(17.5 ± 2.9) μm] [(24.1 ± 3.6) μm] 0.01]. Conclusion Local injection of ILK into the infarcted myocardium may enhance the cardiac function of the infarcted rats, which may be related to the improvement of the angiogenesis and collagen content in the infarcted area and the alleviation of tissue ischemia.