曹青, 王飞, 林继先, 陈书艳. 骨髓间充质干细胞体外对H2O2损伤大鼠心肌细胞的保护[J]. 心脏杂志, 2010, 22(1): 33-36.
    引用本文: 曹青, 王飞, 林继先, 陈书艳. 骨髓间充质干细胞体外对H2O2损伤大鼠心肌细胞的保护[J]. 心脏杂志, 2010, 22(1): 33-36.
    Role of bone mesenchymal stem cells in protection of cardiomyocyte apoptosis by H2O2[J]. Chinese Heart Journal, 2010, 22(1): 33-36.
    Citation: Role of bone mesenchymal stem cells in protection of cardiomyocyte apoptosis by H2O2[J]. Chinese Heart Journal, 2010, 22(1): 33-36.

    骨髓间充质干细胞体外对H2O2损伤大鼠心肌细胞的保护

    Role of bone mesenchymal stem cells in protection of cardiomyocyte apoptosis by H2O2

    • 摘要: 目的: 观察骨髓间充质干细胞(bone mesenchymal stem cells,BMSC)对过氧化氢(H2O2)诱导乳鼠心肌细胞凋亡蛋白Bcl-2家族的影响。方法: 培养新生大鼠的心肌细胞,分为3组,即对照组、模型组和BMSC处理组。用Transwell小室建立心肌细胞与BMSC共培养体系,分别于培养12、24和48 h,采用MTT比色法检测单孔细胞的存活率;用Western blot法检测凋亡蛋白Bcl-2和Bax的表达。结果: 模型组细胞和BMSC处理组细胞在H2O2的诱导下出现细胞凋亡。造模12 h后,模型组细胞的存活率明显低于对照组(P<0.05);BMSC处理组细胞的存活率与模型组相比无明显差异。造模24 h和48 h后,BMSC处理组细胞的存活率与模型组差异明显(P<0.05)。造模12 h后,Bax和Bcl-2蛋白的表达无明显变化。造模24 h后,BMSC处理组细胞中Bax蛋白的表达明显低于模型组(P<0.05),Bcl-2蛋白的表达虽有变化,但无统计学意义。结论: BMSC可调控心肌细胞线粒体凋亡途径,减轻氧自由基对心肌细胞的损伤,其抑制凋亡的作用可能是通过下调Bax蛋白的表达而实现的。

       

      Abstract: AIM: To observe the influence of cell apoptosis-related protein Bcl-2 family on H2O2-treated cardiac myocytes from neonatal rats by bone mesenchymal stem cells (BMSC). METHODS: Cardiac myocytes from neonatal rats were cultured and divided into three groups: control group, model group and BMSC-treated group. Transwell inserts were used for setting up co-culture system between cardiac myocytes and BMSC. MTT colorimetry was used to detect the cellular survival rate separately at 12, 24 and 48 h. Expression of cell apoptosis protein including Bcl-2 and Bax was examined by Western blot. RESULTS: Twelve hours after H2O2 treatment, the cell survival rate in model group was lower than in control group (P<0.05). There was no difference between model group and BMSC-treated group. Cellular survival rates of model group and BMSC-treated group were significantly different at 24 and 48 h. Twelve hours after H2O2 treatment, no difference was found in the expression level of Bax and Bcl-2 among the three groups. Bax expression in BMSC-treated group was significantly down-regulated at 24 h compared with model group (P<0.05). Although Bcl-2 expression was altered, there was no statistically significant difference. CONCLUSION: BMSC decrease myocyte apoptosis after damage from oxygen-derived free radicals, which may result from the down-regulation of Bax expression.

       

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