| 李霜1 吴昊2 张荣庆1 李聪叶1 张铮1 曹丰1.瑞舒伐他汀促进缺氧复氧间充质干细胞增殖的机制研究[J].,2011,11(9):1667-1669 |
| 瑞舒伐他汀促进缺氧复氧间充质干细胞增殖的机制研究 |
| Rosuvastatin Prevents Adipose-derived Mesenchymal Stem Cells fromHypoxia/Reoxygenation Injury through Activation of ERK and AKT |
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| DOI： |
| 中文关键词: 瑞舒伐他汀 间充质干细胞 缺氧复氧损伤 Akt Erk |
| 英文关键词: Rosuvastatin Adipose-derived mesenchymal stem cells Hypoxia/reoxygenation injury Akt Erk |
| 基金项目:国家自然科学基金（30970845）西京医院助推计划重大项目(XJZT08Z04) |
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| 中文摘要: |
| 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、10-6 mol/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)。Western
blot 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。 |
| 英文摘要: |
| Objective: To investigate the effects of Rosuvastatin on the proliferation of adipose-derived mesenchymal stem cells
（AD-MSCs）after hypoxia/reoxygenation (H/R) injury. Methods: AD-MSCs were isolated from Kunming mice and characterized by
flowcytometry. AD-MSCs were divided into three groups: (1) control,(2) Hypoxia 6hrs+ Reoxygen 42hrs (H/R), (3) H/R＋Rosuvastatin
(10-8，10-7，10-6mol/L respectively). Cell proliferation was detected by MTT assays. The protein expressions of Akt, Akt, Erk and pErk
were analyzed by Western blot assay. Results: The CD44 and CD90 of AD-MSCs were positive. Administration of Rosuvastatin increased
proliferation of AD-MSCs after H/R injury (P<0.05). Western blot assay revealed that the levels of phosphorylated Akt and phosphorylated
Erk were higher in Rosuvastatin group than that in H/R group. Conclusion: Rosuvastatin promoted the proliferation of
AD-MSCs after H/R injury by AKT and ERK. |
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