论文部分内容阅读
目的:探讨脂肪来源的干细胞(ADSC)移植对大鼠脑缺血后微血管生成的可能机制。方法:72只清洁级成年雄性Sprague-Darley大鼠,随机分为假手术组(Sham组)、局灶性脑缺血组(MCAO组)、溶剂对照组(vehicle组)和ADSC治疗组(ADSC组),每组18只,采用改良Zea-Longa线栓法制作大脑中动脉栓塞(MCAO)模型,ADSC移植前用DAPI标记,ADSC组于造模成功1d后经侧脑室注射入30μL的经DAPI标记的ADSC细胞悬液,内含1×106细胞,vehicle组则注射同等剂量的PBS,术后4d、7d和14d分批处死实验动物,并断头取脑,采用免疫组织化学法和半定量RT-PCR法检测缺血区脑组织的新生血管及bFGF和VEGF表达的动态变化。结果:大鼠脑缺血后缺血区即可见大量的微血管生成,2周达高峰。ADSC组较MCAO组和vehicle组缺血区微血管密度明显增高(P<0.01);ADSC组术后4d、7d和14d脑组织中bFGF和VEGF的表达水平较MCAO组和vehicle组明显增高。结论:ADSC移植促进脑缺血大鼠缺血区微血管的生成,其机制可能与促进bFGF和VEGF的表达有关。
Objective: To investigate the possible mechanism of adipose-derived stem cell (ADSC) transplantation on micro-angiogenesis after cerebral ischemia in rats. Methods: Seventy-two adult male Sprague-Darley rats were randomly divided into sham operation group (Sham group), focal cerebral ischemia group (MCAO group), solvent control group (vehicle group) and ADSC treatment group (ADSC (N = 18). The middle cerebral artery occlusion (MCAO) model was made by the modified Zea-Longa method. DAPI was used to label the ADSC before transplantation. After ADDA was injected into the lateral ventricle for 1 day, 30μL DAPI Labeled ADSC cell suspension containing 1 × 106 cells, vehicle group injected with the same dose of PBS, 4d, 7d and 14d after the experimental animals were killed in batches, and decapitated brain, immunohistochemical and semi-quantitative The dynamic changes of neovascularization, bFGF and VEGF expression in brain tissue were detected by RT-PCR. Results: A large number of microvessels were found in the ischemic area after cerebral ischemia in rats, reaching the peak at 2 weeks. Compared with MCAO group and vehicle group, the microvessel density of ischemic area in ADSC group was significantly increased (P <0.01). The expression of bFGF and VEGF in ADSC group was significantly higher than that in MCAO group and vehicle group at 4 d, 7 d and 14 d after operation. CONCLUSION: ADSC transplantation can promote angiogenesis of ischemic microvessel in rats with cerebral ischemia, the mechanism may be related to promoting the expression of bFGF and VEGF.