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目的探讨前凋亡因子Bim是否参与血管紧张素Ⅱ诱导的内皮祖细胞(EPCs)调亡及其机制。方法采集人脐静脉血,用6%羟乙基淀粉沉降和密度梯度离心法联合提取脐血中单个核细胞,培养7d,采用免疫荧光法和免疫组化法鉴定EPCs。AngII诱导EPCs凋亡,加入AT受体拮抗剂1h后即刻加入AngII。实验分为对照组、AngⅡ组和AngⅡ+AT受体拮抗剂组。24h后检测EPCs凋亡率,RT-PCR法分析各组BimmRNA的表达。结果一定剂量AngII可诱导EPCs凋亡,通过AT受体拮抗剂的阻断可降低EPCs凋亡率,RT-PCR显示BimmRNA在对照组中低表达,AngⅡ组表达最高,AngⅡ+AT受体拮抗剂组中表达水平显著降低,其表达变化趋势与EPCs凋亡率变化一致。结论 AngⅡ可诱导EPCs凋亡,BIM参与并促进了EPCs的凋亡。
Objective To investigate whether Bim, a proapoptotic factor, is involved in the apoptosis of endothelial progenitor cells (EPCs) induced by angiotensin Ⅱ and its mechanism. Methods Human umbilical cord blood was harvested and mononuclear cells of umbilical cord blood were extracted by 6% hydroxyethyl starch sedimentation and density gradient centrifugation. The cells were cultured for 7 days. EPCs were identified by immunofluorescence and immunohistochemistry. EPCs apoptosis was induced by Angll and AngII was added immediately after adding AT receptor antagonist. The experiment was divided into control group, AngⅡgroup and AngⅡ + AT receptor antagonist group. The apoptotic rate of EPCs was detected 24h later, and the expression of BimmRNA in each group was analyzed by RT-PCR. Results Apoptosis of EPCs was induced by a dose of AngII. The apoptosis rate of EPCs was decreased by blockade of AT receptor antagonist. RT-PCR showed that Bim mRNA was low in the control group and highest in AngⅡ group. AngⅡ + AT receptor antagonist The expression level in the group was significantly lower, and the trend of its expression was consistent with that of EPCs. Conclusion AngⅡ can induce apoptosis of EPCs, BIM is involved in and promote the apoptosis of EPCs.