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目的:建立一种改良的可用于小鼠的慢性心肌缺血模型,并探讨其诱导血管生成的作用机制。方法:采用C57BL/6小鼠构建重复短暂心肌缺血手术模型。心电图和心脏超声对心功能进行监测;常规HE染色评价心肌缺血,血管性假血友病因子(vWF)免疫组化,血小板-内皮细胞黏附分子(CD31)、α平滑肌肌动蛋白(α-SMA)免疫荧光染色评价血管生成情况;同时Western Blot检测血管内皮生长因子(VEGF)表达情况。结果:与假手术组相比,模型组小鼠的心功能没有明显下降(P>0.05),HE染色表明左室心肌处于缺血状态,免疫组化显示血管生成情况明显增加,同时VEGF表达也明显上调(P均<0.05)。结论:成功构建了基于小鼠的慢性心肌缺血诱导血管生成模型,且其促进血管生成的机制可能与上调VEGF表达有关。
OBJECTIVE: To establish a modified model of chronic myocardial ischemia in mice and to explore its mechanism of angiogenesis. Methods: C57BL / 6 mice were used to establish the model of repeated myocardial ischemia. Cardiac function was monitored by electrocardiogram (ECG) and echocardiography. The expression of vWF immunohistochemistry, platelet-endothelial cell adhesion molecule (CD31), alpha-smooth muscle actin SMA) immunofluorescence staining angiogenesis; at the same time Western Blot detection of vascular endothelial growth factor (VEGF) expression. Results: Compared with the sham-operation group, the cardiac function of the model group did not decrease significantly (P> 0.05). The HE staining showed that the left ventricular myocardium was in the ischemic state and the immunohistochemistry showed that the angiogenesis was significantly increased Obviously up-regulated (all P <0.05). CONCLUSION: A mouse model of chronic myocardial ischemia-induced angiogenesis was successfully constructed and its mechanism of promoting angiogenesis may be related to the up-regulation of VEGF expression.