| 尹力 叶雪瑞 刘新新 刘芳 于波.Sirt3对过氧化氢诱导的骨髓间充质干细胞凋亡的保护作用[J].现代生物医学进展英文版,2015,15(31):6039-6042. |
| Sirt3对过氧化氢诱导的骨髓间充质干细胞凋亡的保护作用 |
| Protective Effect of Sirt3 on Mesenchymal StemCells Injured by HydrogenPeroxide |
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| DOI： |
| 中文关键词: 去乙酰化酶3 亲环蛋白d 骨髓间充质干细胞 凋亡 过氧化氢 |
| 英文关键词: Sirt3 Cyclophilin d Mesenchymal stemcells Apoptosis Hydrogen peroxide |
| 基金项目: |
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| 中文摘要: |
| 目的：通过调控骨髓间充质干细胞（mesenchymal stemcells, MSCs）中的Sirtuin-3(Sirt3)蛋白的表达水平，阐明Sirt3对过氧化
氢（H2O2）诱导MSCs 凋亡的保护作用及其机制。方法：将大鼠MSCs 分为正常对照组、H2O2刺激组、H2O2+ Sirt3 转染组、H2O2 +
Sirt3 siRNA 转染组。利用Western blot法检测Sirt3 及cyclophilin d 蛋白的表达水平、利用免疫沉淀法检测cyclophilin d乙酰化水
平、利用流式细胞仪检测细胞凋亡。结果：①H2O2刺激使MSCs 中Sirt3 表达水平降低。②转染Sirt3 可减少H2O2诱导的MSCs的
凋亡，而转染Sirt3 siRNA可增加H2O2诱导的MSCs的凋亡。③Sirt3蛋白的含量并不影响cyclophilin d的表达，但影响cyclophilin d
的乙酰化水平。结论：Sirt3 可能通过减少线粒体通透性转换孔（mitochondrial permeablity transition pore，mPTP）中的关键蛋
白cyclophilin d的乙酰化水平，进一步抑制mPTP的开放，从而减少H2O2诱导的MSCs 的凋亡。 |
| 英文摘要: |
| Objective:To investigate the protective effect and mechanism of Sirt3 on apoptosis induced by hydrogen peroxide
(H2O2) in MSCs by regulating the protein Sirt3 expression level.Methods:The rat MSCs were divided into 4 groups, respectively as normal
control group, H2O2 stimulation group, H2O2 + Sirt3 transfection group, H2O2 + Sirt3 siRNA transfection group. The protein expression
levels of Sirt3 and cyclophilin d were examined by Western blot and the acetylation level of cyclophlin d was examined by immunoprecipitation
assay. Cells apoptosis was measured by flow cytometry.Results:① The expression of Sirt3 decreased compared with control
group after H2O2 stimulation. ② The apoptotic ratio of cells was decreased after transfection of Sirt3, meanwhile, the apoptotic ratio of
cells was improved after transfection of Sirt3 siRNA. ③ The acetylation level of cyclophilin d but not the expression level of protein cyclophilin
d was influenced by regulating the protein Sirt3 expression level.Conclusion:Sirt3 might have an apoptosis-protective effect
on MSCs induced by H2O2 though reducing opening of mPTP by deacetylateing cyclophilin d. |
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