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目的:探讨瑞舒伐他汀对缺氧复氧损伤后脂肪来源间充质干细胞增殖的影响及机制。方法:酶消化法分离小鼠的脂肪间充质干细胞(AD-MSCs),流式细胞术检测CD90、CD44、CD34、CD45等细胞标志物。建立缺氧(H)6h/复氧(R)42h细胞模型,AD-MSCs分为3组:①对照组;②缺氧/复氧组(H/R);③H/R+瑞舒伐他汀干预组(浓度分别为10-8、10-7、10-6mol/L)。MTT法测定各组细胞增殖,免疫印迹法检测细胞内Akt、Erk及其磷酸化的表达水平。结果:流式细胞术结果显示脂肪间充质干细胞CD44及CD90阳性,CD34、CD45阴性。MTT实验显示在缺氧环境中,瑞舒伐他汀的干预可显著增加AD-MSCs的增殖(P<0.05)。Westernblot检测pAkt及pErk的表达在瑞舒伐他汀干预组明显高于对照组和H/R组。(P<0.05)。结论:瑞舒伐他汀可通过Akt、Erk信号途径促进H/R损伤后AD-MSCs的增殖。
Objective: To investigate the effect of rosuvastatin on proliferation of adipose-derived mesenchymal stem cells after hypoxia-reoxygenation injury and its mechanism. Methods: Adipose-derived mesenchymal stem cells (AD-MSCs) were isolated by enzymatic digestion. Cell markers such as CD90, CD44, CD34 and CD45 were detected by flow cytometry. To establish a cell model of hypoxia (H) 6h / reoxygenation (R) 42h, AD-MSCs were divided into three groups: ①control group; ②oxia / reoxygenation group Group (concentrations were 10-8,10-7,10-6 mol / L respectively). Cell proliferation was measured by MTT assay. The expression of Akt, Erk and phosphorylation were detected by Western blotting. Results: The results of flow cytometry showed that CD44 and CD90 were positive in adipose-derived mesenchymal stem cells, but negative in CD34 and CD45. MTT experiments showed that rosuvastatin intervention significantly increased the proliferation of AD-MSCs in hypoxic environment (P <0.05). Western blot analysis showed that the expression of pAkt and pErk in rosuvastatin intervention group was significantly higher than that in control group and H / R group. (P <0.05). Conclusion: Rosuvastatin can promote the proliferation of AD-MSCs after H / R injury through Akt, Erk signaling pathway.