中文摘要：

目的：探讨人趋化素样因子1（chemokine-like factor1,CKLF1）基因转移对急性心肌梗死大鼠梗死面积及心功能的影响。方法：雄性3月龄Sprague-Dawley（SD）大鼠30只,随机分为3组,盐水组、CKLF1组、空质粒组,分别于股直肌内注射生理盐水100μg、CKLF1真核表达质粒或空载质粒100μg,并予以直流方波电脉冲刺激,第6天结扎冠状动脉前降支构建大鼠急性心肌梗死模型,第22天行超声心动图及血流动力学检查,然后处死大鼠,测定心肌梗死面积。结果：CKLF1组,左心室射血分数（67.02%±12.24%）明显高于盐水组（43.64%±7.82%）及空质粒组（47.56%±4.10%）,P〈0.05;左心室短轴缩短率（33.83%±10.15%）明显高于盐水组（18.49%±3.96%）及空质粒组（20.85%±2.24%）,P〈0.05;左心室压力上升最大速率[（5720.01±826.32）mmHg/s,1mmHg=0.133kPa]明显高于盐水组[（3955.69±685.91）mmHg/s]及空质粒组[（4412.03±500.74）mmHg/s],P〈0.05;左心室压力下降最大速率[（4636.23±407.17）mmHg/s]明显高于盐水组[（2984.82±615.24）mmHg/s]及空质粒组[（2963.87±419.36）mmHg/s],P〈0.05;而CKLF1组大鼠心肌梗死面积（29.63%±3.93%）明显小于盐水组（38.01%±5.48%）及空质粒组（37.50%±6.33%）,P〈0.05。结论：CKLF1基因转移可以缩小大鼠心肌梗死面积并改善其心功能。

英文摘要：

Objective ： To study the effects of chemokine-like factor 1 （ CKLF1 ） -plasmid transfer on cardiac function in a rat acute myocardial infarction （AMI） model. Methods： Thirty male SD rats were randomly devided into 3 groups. One hundred micrograms of CKLF1-plasmid, empty plasmid or saline were injected intramuscularly with in vivo eleetroporation, respectively. Rats were subjected to left coronary artery ligation on the 6th day after gene transfer. Ultrasonic cardiography and hemodynamics were conducted and evaluated on the 22nd day after gene transfer. Then, the animals were sacrificed for determination of percentage of myocardial infareion. Results ： The left ventricular ejection fraction in CKLF1 group （67.02% ± 12.24% ） was significantly higher than that in the saline group （43.64% ±7. 82% ） and empty plasmid group （47.56% ±4. 10% ）, P 〈0.05. Fractional shortening of left ventricle in CKLF1 group （33.83% ± 10. 15% ） was higher than that in saline group （ 18.49% ± 3.96% ） and empty plasmid group （20. 85% ± 2.24% ）, P 〈 0.05. The maximal velocity of left ventricular pressure ascensus was higher in CKLF1 group [ （5 720. 01± 826.32） mmHg/s, 1 mmHg = 0. 133 kPa ] than in saline group[ （3 955.69 ±685.91） mmHg/sl and in empty plasmid group [（4 412.03 ± 500.74） mmHg/s） ] , P 〈 0. 05. And the maximal velosity of left ventricular pressure descensus was higher in CKLF1 group [ （4 636.23 ±407.17） mmHg/s] than in saline group [ （2 984. 82 ±615.24） mmHg/s] and in empty plasmid group [ （2 963.87 ±419.36） mmHg/s], P 〈0.05. While the percentage of myocardial infarction in CKLF1 group （29. 63% ±3.93% ） was smaller than that in saline group （38. 01% ±5.48% ） and in empty plasmid group （37.50% ± 6.33% ） , P 〈 0. 05. Conclusion： CKLF1 gene transfer can limit the mass of myocardial infarction and improve post-infarction cardiac function.