糖尿病心肌缺血大鼠骨髓干细胞动员及心肌组织细胞因子的表达

发布时间：2018-04-15 05:07

本文选题：心肌缺血 + 糖尿病　；参考：《西安交通大学学报(医学版)》2017年01期

【摘要】：目的探讨糖尿病心肌缺血大鼠外周血骨髓干细胞动员和归巢的变化以及缺血心肌组织中血管内皮生长因子和肿瘤坏死因子α的表达变化。方法首先采用链脲佐菌素腹腔注射建立雄性SD大鼠糖尿病模型,然后通过开胸结扎冠状动脉左前降支建立糖尿病心肌缺血模型,并分为缺血1d组、缺血3d组、缺血7d组、缺血28d组;另设相应时间点的糖尿病对照组(开胸但不进行动脉结扎)和正常对照组(不进行腹腔注射和动脉结扎),每组6只。应用流式细胞术测定各组大鼠的外周血单个核细胞中CD34+细胞百分率;应用免疫组化法观察各组动物缺血心肌中CD34+细胞归巢以及血管内皮生长因子和肿瘤坏死因子α的表达。结果大鼠糖尿病心肌缺血组于术后出现骨髓干细胞动员,1周内达高峰,随时间延长减弱;同时术后1周内缺血心肌组织中相应地出现骨髓干细胞归巢以及血管内皮生长因子和肿瘤坏死因子α表达明显增加。结论糖尿病缺血心肌早期可通过组织局部血管内皮生长因子和肿瘤坏死因子α表达升高而动员骨髓干细胞进入外周血,并归巢至缺血心肌,从而启动自体保护机制。
[Abstract]:Objective to investigate the changes of bone marrow stem cell mobilization and homing in diabetic rats with myocardial ischemia and the expression of vascular endothelial growth factor (VEGF) and tumor necrosis factor 伪 (TNF- 伪) in ischemic myocardium.Methods Diabetic model of male SD rats was established by intraperitoneal injection of streptozotocin, and then myocardial ischemia model was established by ligation of left anterior descending coronary artery. The model was divided into 1 day ischemia group, 3 day ischemia group and 7 day ischemia group.There were 6 rats in each group in the control group with diabetes (open chest but no artery ligation) and the normal control group (no intraperitoneal injection and artery ligation) at the same time.The percentage of CD34 cells in peripheral blood mononuclear cells (PBMC) and the homing of CD34 cells and the expression of vascular endothelial growth factor (VEGF) and tumor necrosis factor- 伪 (TNF- 伪) in ischemic myocardium were determined by flow cytometry.Results in the diabetic myocardial ischemia group, the mobilization of bone marrow stem cells reached the peak within 1 week after operation, and decreased with the prolongation of time.The homing of bone marrow stem cells and the expression of vascular endothelial growth factor (VEGF) and tumor necrosis factor- 伪 (TNF- 伪) were also found in ischemic myocardium one week after operation.Conclusion early diabetic ischemic myocardium can mobilize bone marrow stem cells to enter peripheral blood and homing to ischemic myocardium by increasing the expression of vascular endothelial growth factor and tumor necrosis factor- 伪, thus initiating the mechanism of autoprotection.
【作者单位】：西安交通大学第一附属医院老年病科;西安交通大学第一附属医院心内科;
【基金】：国家自然科学基金资助项目(No.81200098) 陕西省自然科学基金项目(No.2014K11-03-04-06)~~
【分类号】：R587.2;R541

【相似文献】