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目的观察ALT711干预对大鼠骨髓内皮祖细胞(endothelial progenitor cells,EPCs)活性的影响,探讨ALT711影响年龄导致的EPCs功能改变的可能机制及在细胞移植治疗损伤性血管疾病中的作用。方法3~4月龄、10~12月龄、18~20月龄3个年龄段大鼠,每个年龄段20只随机分为ALT711喂养组和对照组(n=10),从骨髓获取单个核细胞并进行体外培养、分化。培养7d后检测各组EPCs迁移、黏附、增殖能力。提取3个年龄段大鼠血清,分为ALT711干预组和对照组培养年轻大鼠骨髓EPCs,培养7d后检测培养的各组EPCs迁移、黏附、增殖能力。结果随供体大鼠年龄增加,骨髓EPCs迁移[(30.5±2.0)vs(18.8±2.3)vs(12.9±1.6)EPCs/视野(×400),P<0.01]、黏附[(52.2±2.3)vs(31.5±3.3)vs(23.9±2.0)EPCs/视野(×400),P<0.01]、增殖[(0.522±0.031)vs(0.349±0.022)vs(0.272±0.020),P<0.01]能力降低,使用ALT711干预可恢复因供体年龄增加导致的骨髓活性减弱;随供体大鼠年龄增加其血清对培养的年轻供体骨髓EPCs迁移[(26.8±1.8)vs(20.2±1.5)vs(16.0±1.3)EPCs/视野(×400),P<0.01]、黏附[(45.6±2.1)vs(30.1±3.0)vs(22.8±1.6)EPCs/视野(×400),P<0.01]、增殖[(0.466±0.023)vs(0.360±0.019)vs(0.303±0.015),P<0.01]活性具有抑制作用,加入ALT711干预可以拮抗这种效应。结论EPCs生物学功能随机体年龄增加而减退,ALT711干预可以改善供体增龄导致的EPCs活性减退,拮抗老年供体血清对EPCs活性的负性调节效应。
Objective To investigate the effect of ALT711 on the activity of endothelial progenitor cells (EPCs) in bone marrow of rats, and to explore the possible mechanism of ALT711 on the age-dependent changes of EPCs and the role of ALT711 in the treatment of damaged vascular diseases. Methods Totally 3 rats aged 3 to 4 months, 10 to 12 months and 18 to 20 months old were randomly divided into ALT711 feeding group and control group (n = 10) Nuclear cells and cultured in vitro, differentiation. After 7 days of culture, the migration, adhesion and proliferation of EPCs in each group were detected. The serum of 3 age-matched rats was extracted and divided into ALT711-treated and control groups. EPCs of young rats were cultured. After 7 days of culture, the migration, adhesion and proliferation of EPCs were detected. Results EPCs migrated [(30.5 ± 2.0) vs (18.8 ± 2.3) vs (12.9 ± 1.6) EPCs / FOVs, P <0.01] (P <0.01), (P <0.01), (P <0.01), P <0.01] (26.8 ± 1.8) vs (20.2 ± 1.5) vs. (20.2 ± 1.5), respectively, in the serum of donor donors with increasing age of donors (P <0.01)]. The number of EPCs / visual field (× 400), P <0.01] [(0.466 ± 0.023) vs (0.360 ± 0.019) vs (0.303 ± 0.015), P <0.01], and ALT711 could antagonize this effect. Conclusions The biological function of EPCs decreased with the increase of age. ALT711 treatment could improve the decrease of EPCs activity induced by donor aging and antagonize the negative regulation of EPCs activity by old donor serum.