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目的观察经尾静脉注射携带VEGF基因的MSCs移植对脑梗死模型大鼠血管生成方面的影响。方法采用直接贴壁全骨髓法分离纯化MSCs,通过脂质体转染技术将pIRES2-EGFP-VEGF导入MSCs,另采用改良Zea Longa线栓法将40只SD大鼠制成左侧大脑中动脉栓塞/再灌注模型,并随机分4组:VEGF-MSCs组、MSCs组、PBS组、Model组;造模24 h后Model组不做处理,前3组大鼠分别经尾静脉注射1 ml VEGF-MSCs、MSCs、PBS悬液;细胞移植7d后用免疫组织化学法测定脑梗死周围Ang-2、CD34的表达水平。结果 VEGF-MSCs组和MSCs组Ang-2、CD34阳性表达水平较PBS组、Model组高(P<0.05),且VEGF-MSCs组较MSCs组更高(P<0.05);Model组与PBS组差异不明显(P>0.05)。结论经尾静脉注射携带VEGF基因的MSCs移植入MCAO模型大鼠可以促进缺血脑组织新生血管的形成,其机制可能为VEGF上调缺血周边区域Ang-2、CD34的表达水平。
Objective To observe the effect of transplantation of MSCs carrying VEGF gene via tail vein on the angiogenesis in rats with cerebral infarction. METHODS: MSCs were isolated and purified by direct adherent whole bone marrow. PIRES2-EGFP-VEGF was transfected into MSCs by liposome transfection technique. Forty Sprague Dawley rats were randomly divided into three groups: / Reperfusion model, and randomly divided into 4 groups: VEGF-MSCs group, MSCs group, PBS group, Model group; Model 24 h after model treatment, the first three groups were injected via tail vein injection of 1 ml of VEGF- MSCs, MSCs and PBS suspension. The expression of Ang-2 and CD34 around the cerebral infarction was measured by immunohistochemical method 7 days after cell transplantation. Results The expression of Ang-2 and CD34 in VEGF-MSCs group and MSCs group was higher than PBS group and Model group (P <0.05), and VEGF-MSCs group was higher than MSCs group (P <0.05) The difference was not significant (P> 0.05). Conclusion Transplantation of tail vein-derived MSCs carrying VEGF gene into MCAO model can promote angiogenesis in ischemic brain tissue. The possible mechanism is that VEGF may up-regulate the expression of Ang-2 and CD34 in the peripheral region of ischemic area.