【摘要】 目的研究辛伐他汀对过氧化氢(H2O2)诱导的骨髓间充质干细胞(BMSCs)凋亡的影响,并探讨其可能的机制。方法采用全骨髓贴壁培养法培养SD大鼠BMSCs,随机分成7组:正常对照组(A组)、H2O2处理组(B组)和不同浓度辛伐他汀处理组(C1、C2、C3、C4组,分别为辛伐他汀0.001、0.01、0.1、1μmol/L)及LY294002干预组(D组)。流式细胞术检测各组细胞凋亡率,并用Western blot检测BMSCs中p-Akt、Akt表达。结果与B组比较,辛伐他汀处理组均抑制H2O2诱导的BMSCs凋亡,以C2组抗凋亡作用最为显著(P<0.05);而LY294002(D组)能明显阻断辛伐他汀的抗凋亡效应(P<0.01)。辛伐他汀处理组p-Akt活性显著高于A、B组(P<0.01),而LY294002(D组)阻断p-Akt水平(P<0.01)。结论一定浓度范围内的辛伐他汀能抑制H2O2诱导的BMSCs凋亡,其机制可能与PI3K/Akt信号通路有关。更多还原

【Abstract】 Objective:To investigate the effect of simvastatin on the apoptosis of hydrogen peroxide (H2O2)-induced bone marrow-derived mesenchymal stem cells(BMSCs) and explore its possible mechanism.Methods:BMSCs were isolated from SD rats by whole bone marrow adherence culture method.The cells were randomly divided into 7 groups of A(normal control),B(treated with H2O2),C1(treated with simvastatin 0.001 mol/L),C2(treated with simvastatin 0.01 mol/L),C3(treated with simvastatin 0.1 mol/L),C4(treated with simvastatin 1 mol/L) and D(treated with LY294002).The apoptosis of BMSCs was detected by flow cytometry and the expressions of p-Akt and Akt were analyzed by Western blot.Results:Compared with group B,different concentrations of simvastatin,especially group C2,inhibited H2O2-induced apoptosis of BMSCs(P<0.05),which was significantly blocked by LY294002 in group D(P<0.01).p-Akt activities in groups of C1,C2,C3 and C4 were higher than those in groups of A and B(P<0.01),whereas the level of p-Akt was inhibited in group D(P<0.01).Conclusion:Simvastatin in a definite concentration range can inhibit H2O2-induced apoptosis of BMSCs,which may be related with PI3K/Akt signaling pathway.更多还原