中文摘要：

目的：分析过表达胰岛素样生长因子1（IGF-1）对脐带间充质干细胞（UC-MSCs）氧化损伤的抑制作用,开发UC-MSCs新的应用模式。方法：通过酶消化法,从脐带组织中分离UC-MSCs,并采用流式细胞术对细胞的表面特异标志物进行鉴定,通过逆转录病毒感染体系,构建过表达IGF-1的UC-MSCs（UC-MSCs-IGF-1）,并进一步通过实时荧光定量PCR和流式细胞术对UC-MSCs-IGF-1的IGF-1表达水平进行评价,同时分析UC-MSCs-IGF-1的表面标志物及成骨成脂分化能力;用不同浓度的H_2O_2（0μmol/L、10μmol/L、50μmol/L和100μmol/L）处理细胞,分析UC-MSCs-IGF-1在增殖活力维持、抗氧化损伤和抗凋亡方面的优势。结果：UC-MSCs表面标志物CD29、CD90和CD105的表达均呈阳性,而CD34的表达为阴性,符合正常间充质干细胞的表型特征;实时荧光定量PCR和流式细胞术结果表明,应用逆转录病毒感染体系构建的UC-MSCs-IGF-1在IGF-1表达方面远高于正常UC-MSCs,同时干细胞表型与UC-MSCs一致,且具备正常的成脂成骨分化能力;在H_2O_2的氧化损伤作用下,与UC-MSCs相比,UC-MSCs-IGF-1具有较强的增殖活力和抗氧化、抗凋亡功能,同时细胞中的SOD活性略高于UC-MSCs。结论：过表达IGF-1对UC-MSCs的氧化损伤及氧化引起的凋亡均具有一定的防护作用,与正常UC-MSCs相比,UC-MSCsIGF-1可能在临床应用方面具有一定的优势。

英文摘要：

AIM： To analyze the inhibitory effect of insulin-like growth factor-1（ IGF-1） overexpression in umbilical cord mesenchymal stem cells（ UC-MSCs） on oxidative damage and to develop new application model for UCMSCs. METHODS： UC-MSCs were isolated from human umbilical cord with enzymatic digestion,and further characterized with flow cytometry. IGF-1-overexpressing UC-MSCs（ UC-MSCs-IGF-1） were established by retrovirus infection.IGF-1 expression of UC-MSCs-IGF-1 was evaluated by real-time quantitative PCR and flow cytometry,and its surface markers,as well as osteogenic and adipogenic differentiation ability,were further analyzed. The proliferation,anti-oxidative damage and anti-apoptosis abilities of UC-MSCs-IGF-1 were evaluated when treated with H_2O_2 at different concentrations（ 0μmol /L,10 μmol /L,50 μmol /L and 100 μmol /L）. RESULTS： UC-MSCs showed positive expression of CD29,CD90 and CD105,but negative expression of CD34,which coincided with the normal phenotype of mesenchymal stem cells. UCMSCs-IGF-1 established with retrovirus infection showed much higher expression of IGF-1 compared with normal UC-MSCs,and expressed the same surface markers as UC-MSCs. The osteogenic and adipogenic differentiation abilities were also observed. With the oxidative damage by H_2O_2 treatment,UC-MSCs-IGF-1 showed more strong proliferation,anti-oxidative damage and anti-apoptosis abilities as compared with normal UC-MSCs. In addition,the activity of SOD in UC-MSCs-IGF-1 was a little higher than that in control group. CONCLUSION： IGF-1 overexpression in UC-MSCs inhibits oxidative damage and cell apoptosis. UC-MSCs-IGF-1 may have more advantagies in clinical application.