论文部分内容阅读
目的:探索腺病毒介导的基质细胞衍生因子-1对心肌梗死心脏功能的影响.方法:采用成年SD大鼠,经左冠状动脉前降支结扎建立急性心肌梗死模型.术后1h,将1×1010PFUAdv-SDF-1分6个点注射到心肌梗死部位及其周边区域.移植后4wk测定心脏功能,随后取材、连续冰冻切片,观察CD133和CD31的表达以及心肌组织形态学.结果:注射在心肌梗死部位的Adv-SDF-1高表达,促进了CD133和CD31阳性细胞迁移到心肌梗死部位,增加了心肌梗死部位毛细血管的密度(Ad-SDF-1组与模型组和Ad-LacZ组相比:32±4vs15±2,16±3,P<0.05),保护并促进了心肌再生,从而缩小梗死区域面积,心室壁的厚度和弹性增加;心室胶原含量减少[Ad-SDF-1组与模型组和Ad-LacZ组相比:(41±3)%vs(78±8)%,(76±7)%,P<0.05],延缓心室重构而改善心脏的收缩和舒张功能.结论:SDF-1过表达通过促进血管新生改善心肌的血供,达到改善心脏功能的目的.
Objective: To explore the effect of adenovirus-mediated stromal cell-derived factor-1 on cardiac function in myocardial infarction.Methods: Adult SD rats were established by acute left anterior descending coronary artery ligation to establish acute myocardial infarction model.After 1h, 1 × 1010PFUAdv-SDF-1 was injected into the myocardial infarction site and its peripheral area at 6 points.After 4 weeks of transplantation, the cardiac function was measured and then the frozen sections were harvested for the observation of the expression of CD133 and CD31 and the morphology of myocardial tissue.Results: The high expression of Adv-SDF-1 in the myocardial infarction area promoted the migration of CD133 and CD31 positive cells to the myocardial infarction site and increased the density of capillaries in the myocardial infarction area (Ad-SDF-1 group and Ad-LacZ group 32 ± 4 vs 15 ± 2, 16 ± 3, P <0.05), which protected and promoted myocardial regeneration, thereby reducing infarct size, increasing thickness and elasticity of ventricular wall, and decreasing collagen content in the ventricle Compared with Ad-LacZ group, the model group (41 ± 3)% vs (78 ± 8)%, (76 ± 7)%, P <0.05], delayed ventricular remodeling and improved cardiac contractile and diastolic function. : SDF-1 overexpression improves myocardial function by promoting angiogenesis and improving cardiac function.