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目的:探讨缺氧复氧损伤环境下Ghrelin对脂肪来源的间充质干细胞(AD-MSCs)的保护作用,以寻求AD-MSCs心肌内移植的有利因素。方法:采用胶原酶消化法分离小鼠AD-MSCs,流式细胞术鉴定其标志。建立缺氧/复氧细胞模型,分3组:①对照组;②缺氧/复氧组(H/R);③H/R+Ghrelin(浓度分别为10-9、10-8、10-7mol/L)干预组。MTT法测定各组细胞增殖,TUNEL法检测细胞凋亡。结果:流式细胞术结果显示AD-MSCs CD44及CD90阳性,CD34、CD45阴性。AD-MSCs MTT分析显示在缺氧环境中,Ghrelin相比于单纯H/R组能够显著促进AD-MSCs的存活与增殖,并抑制其凋亡(P<0.05)。结论:Ghrelin可以明显提高缺氧复氧环境下AD-MSCs的生存与增殖,抑制缺氧诱导的凋亡发生,有望为心肌梗死的干细胞移植治疗创造新的有利因素。
AIM: To investigate the protective effect of Ghrelin on adipose-derived mesenchymal stem cells (AD-MSCs) under hypoxia-reoxygenation injury in order to find favorable factors for myocardial transplantation of AD-MSCs. Methods: AD-MSCs were isolated by collagenase digestion and identified by flow cytometry. Hypoxia / reoxygenation group (H / R); H / R + Ghrelin (concentration were 10-9,10-8,10-7 mol / L) intervention group. Cell proliferation was measured by MTT assay and apoptosis by TUNEL assay. Results: Flow cytometry showed that CD44 and CD90 were positive in AD-MSCs, and CD34 and CD45 were negative in AD-MSCs. MTT assay of AD-MSCs showed that Ghrelin could significantly promote AD-MSCs survival and proliferation and inhibit apoptosis (P <0.05) compared with H / R group. CONCLUSION: Ghrelin can significantly increase the survival and proliferation of AD-MSCs under hypoxia-reoxygenation condition and inhibit the hypoxia-induced apoptosis. It is expected that Ghrelin may create new favorable factors for stem cell transplantation for myocardial infarction.