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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。
Objective To study the mechanism of human chemokine-like factor (CKLF) 1 in improving cardiac function after acute myocardial infarction in rats. Methods Eighteen male Sprague-Dawley rats were randomly divided into three groups with 6 rats in each group. Muscle electrotransfer CKLF1 plasmid, empty plasmid and saline. On the sixth day after electrotransformation, a rat model of acute myocardial infarction was established. Rats were killed on the 27th day after electroporation, and the BrdU / α-actin and Ki67 / α-actin immunohistochemical staining. Results The number of BrdU positive cells in the peripheral zone of CKLF1 group was significantly higher than that in saline group and empty plasmid group (33.11 ± 2.10 / high power field vs 14.16 ± 1.63 / high power field, 18.46 ± 2.77 / high power field, P <0.05) The Ki67 positive cells in the peripheral infarction area were significantly more than those in saline group and empty plasmid group (35.20 ± 8.06 / high power field ratio of 15.96 ± 3.58 / high power field, 17.52 ± 2.66 / high power field, P <0.05). There was no significant difference in each index between saline group and empty plasmid group. Conclusion CKLF1 can promote rat myocardial cell proliferation after myocardial infarction.