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| 二甲基乙二酰基甘氨酸对小鼠骨髓间充质 干细胞缺血清凋亡及Bcl-2/Bax蛋白表达 的影响 |
| Effect of dimethyloxalglycine on the apoptosis induced by serum deprivation and expression of Bcl-2/Bax in mouse bone marrow mesenchymal stem cells |
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| DOI： |
| 中文关键词: 脯氨酸羟化酶抑制剂 二甲基乙二酰基甘氨酸 骨髓间充质干细胞 凋亡 |
| 英文关键词:Prolyl hydroxylase inhibiLors Dmiethyloxalglycine Bone marrow mesenchymal stem cell Apoptosis |
| 基金项目:云南省卫生厅科研基金（2011WS0033 ) |
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| 中文摘要: |
| 目的观察脯氨酸羟化酶抑制剂二甲基乙二酰基甘氨酸（dimeLhyloxalglycine，DM0G )对无血 清培养引起的小鼠骨髓间充质干细胞的凋亡影响及其对凋亡调控蛋白Bci-2/Bax表达的影响。方法 分离小鼠股骨及胫骨骨髓腔中的单个核细胞，传代后应用流式细胞仪进行细胞表型检测和三系分 化以鉴定骨髓间充质干细胞。流式细胞仪TUNEL法观察DMOG作用于细胞后对细胞无血清培养凋 亡的对抗作用，WesLerm bloL检测DM0G对凋亡调控蛋白Bci-2/Bax蛋白表达的影响。结果实验所 获的单个核细胞通过流式细胞仪细胞表型鉴定和三系分化鉴定证实为骨髓间充质干细胞。与无血清 造模组相比，二甲基乙二酰基甘氨酸能明显降低骨髓间充质干细胞因缺血清导致的凋亡率（p<0.05 )，并上调凋亡抑制蛋白Bcl-2蛋白表达（P <0. 05 )，抑制凋亡促进蛋白Bax蛋白表达（P <0. 05 )。结论脯氨酸羟化酶抑制剂阅酝0郧能抑制骨髓间充质干细胞因缺血清培养引起的凋亡。对凋亡调 控蛋白Bci-2/Bax表达的调控可能是DM0G对抗骨髓间充质干细胞凋亡的重要机制。 |
| 英文摘要: |
| Objective To evaluate the effect of prolyl hydroxylase inhibitor，dmiethyloxalglycine ( DMOG )， on the apoptosis of mouse bone marrow niesenchymal steni cells ( BMSCs ) induced by serum deprivation and the expression of apoptosis regulation proteins, Bcl-2/Bax. Methods Mononuclear cells in Lhe caviLy of the emur and tibia in mice were isolated. After passaging， cell phenotype was identified using ilow cytometry.BMSCs were identified using tri-lineage differentiation. The effect of DOMG on the apoptosis induced by serum deprivation was assessed using TUNEL sLaining and fkm cytometry. The expression of Bcl-2/Bax was evaluated with WesLern blotting. Results The mononuclear cells isolaLed in this experiment were identified as BMSCs using flow cytomeLry for cell phenotype and tri-lineage identification. Compared to serum-free modeling group，DM0G could obviously reduce the apoptosis raLe of BMSCs induced by serum deprivation (p < 0. 05 )， up-regulate the expression of Bcl-2 pro Lein (p < 0. 05 )， and down-regulate the expression of Bax proLein (p < 0. 05 ). Conclusion Prolyl hydroxylase inhibiLor DMOG can inhibiL the apoptosis of BMSCs induced by serum deprivation. The regulaLion of the expression of Bcl-2/Bax may be an miportant mechanism of the anti-apoptotic effect of DMOG on BMSCs. |
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