中文摘要：

目的初步研究人趋化素样因子（CKLF）1改善大鼠急性心肌梗死后心功能的机制。方法选取18只雄性SD大鼠,随机分为三组,每组6只,分别肌肉电转CKLF1质粒、空质粒及盐水。电转后第6天构建大鼠急性心肌梗死模型。电转后第27天处死大鼠,行BrdU/α-actin、Ki67/α-actin免疫组化染色。结果CKLF1组梗死周边区BrdU阳性细胞明显多于盐水组及空质粒组（33.11±2.10个/高倍视野比14.16±1.63个/高倍视野、18.46±2.77个/高倍视野,P〈0.05）;CKLF1组梗死周边区Ki67阳性细胞明显多于盐水组及空质粒组（35.20±8.06个/高倍视野比15.96±3.58个/高倍视野、17.52±2.66个/高倍视野,P〈0.05）。盐水组与空质粒组相比,各指标差异无统计学意义。结论CKLF1可以促进心肌梗死后大鼠心肌细胞增殖。

英文摘要：

Objective To study the mechanism of CKLF1-plasmid transfer on the myocardial repair in rat AMI models. Methods Eighteen male SD rats were randomly divided into 3 groups and in each separate group, the rats were injected intramuscalary with plasmid DNA encoding CKLF1 geue （ n = 6） , emptyplasmid （n =6） and saline （n = 6） with in vivo electroporation respectively. Rats were subjected to left coronary artery ligation on the 6th day after gene transfer and were killed on the 21st day. The expressions of BrdU/α-actin, Ki67/α-actin were assessed by immunohistochemistry. Results BrdUpositive cells in CKLFI group were more than those in the saline group and the empty plasmid group （cells/ HP） （33. 11 ±2. 10 vs. 14. 16 ± 1.63 ＆ 18.46 ±2. 77, P 〈0. 05）. Ki67-positive ceils in the CKLF1 group were more than those in the saline group and the empty plasmid group （cells/HP） （35.20 ± 8.06 vs. 15.96±3.58 ＆ 17.52 ±2. 66, P 〈0. 05 ）. But there was no significance between the empty plasmid group and the saline group （ P 〉 0. 05）. Conclusion Intramuscular injection with in vivo eleetroporation of CKLF1 may cause an enhanced myocardial proliferation of acute myocardial infarction tissue in experimental rat.