中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (6): 955-958.doi: 10.3969/j.issn.1673-8225.2011.06.002

• 骨髓干细胞 bone marrow stem cells • 上一篇    下一篇

低氧增强骨髓间充质干细胞对缺氧诱导心肌细胞凋亡的可能性

周美玲，王爱玲，徐  凤，陈  峰   

  1. 安徽医科大学第一附属医院心内科，安徽省合肥市  230022
  • 收稿日期:2010-08-01 修回日期:2010-11-20 出版日期:2011-02-05 发布日期:2011-02-05
  • 通讯作者: 王爱玲，硕士，主任医师，教授，博士生导师，副主任，安徽医科大学第一附属医院心血管内科，安徽省合肥市 230022 wal2010@yahoo.cn
  • 作者简介:周美玲★，女，1982年生，安徽省安庆市人，汉族，安徽医科大学在读硕士，主要从事间充质干细胞对缺血性疾病的作用的研究。 zener2000@163.com

Probability of bone marrow mesenchymal stem cells enhanced by hypoxia precondition against cardiomyocyte apoptosis induced by hypoxia

Zhou Mei-ling, Wang Ai-ling, Xu Feng, Chen Feng   

  1. Department of Cardiology, First Affiliated Hospital, Anhui Medical University, Hefei  230022, Anhui Province, China
  • Received:2010-08-01 Revised:2010-11-20 Online:2011-02-05 Published:2011-02-05
  • Contact: Wang Ai-ling, Master, Chief physician, Professor, Doctoral supervisor, Department of Cardiology, First Affiliated Hospital, Anhui Medical University, Hefei 230022, Anhui Province, China wal2010@yahoo.cn
  • About author:Zhou Mei-ling★, Studying for master’s degree, Department of Cardiology, First Affiliated Hospital, Anhui Medical University, Hefei 230022, Anhui Province, China zener2000@163.com

PDF

398

被引次数

10

摘要：

背景：骨髓间充质干细胞移植入缺血心肌后存活率低，而低氧有可能增强骨髓间充质干细胞的增殖，促进其存活。
目的：体外模拟心肌细胞缺血微环境，探索低氧预处理后，骨髓间充质干细胞对持续缺氧诱导的心肌细胞凋亡的保护作用。
方法：取第4代SD大鼠骨髓间充质干细胞用于制备条件培养液。取胚胎大鼠心肌细胞株，随机分成4组：对照组：心肌细胞正常培养组；模型组：心肌细胞单纯缺氧；骨髓间充质干细胞组：心肌细胞与骨髓间充质干细胞条件培养液共缺氧；低氧组：心肌细胞与骨髓间充质干细胞低氧条件培养液共缺氧。MTT检测各组细胞活力变化，Annexin V-FITC双染标记心肌细胞凋亡，免疫组化检测各组Bax和Bcl-2蛋白的表达。
结果与结论：免疫组化显示，低氧组的Bcl-2表达较其他各组增强，而Bax的表达比模型组和骨髓间充质干细胞组减弱，Bcl-2/Bax比值最大。与对照组和骨髓间充质干细胞组相比，低氧组的细胞活力高(P < 0.05)，凋亡率降低(P < 0.05)。提示低氧可能是通过增强旁分泌机制，从而对Bax和Bcl-2进行调节，对心肌细胞凋亡有保护效应。

关键词: 缺氧, 心肌细胞, 骨髓间充质干细胞, 移植, 凋亡

Abstract:

BACKGROUND: Bone marrow mesenchymal stem cells (BMSCs) have a lower survival rate after implanted into the ischemic myocardium. However, hypoxia precondition may enhance BMSCs proliferation and promote its survival rate.
OBJECTIVE: To stimulate the micro-environment of myocardial ischemia in vitro, and to investigate the protective effect of BMSCs on cardiomyocytes apoptosis continually induced by hypoxia after the hypoxia precondition (HP).
METHODS: The 4th passage SD rats BMSCs were used to prepare conditioned medium. Embryonic cardiomyocytes from rats were randomly divided into 4 groups: cardiomyocytes culture under normal condition alone (normal group), cardiomyocytes culture under hypoxia condition alone (model group), cardiomyocytes co-cultured with conditioned medium of BMSCs under normal condition (BMSCs group), cardiomyocytes co-cultured conditioned medium of BMSCs under hypoxia precondition (HP group). Changes in cell viability were measured by MTT assay, cardiomyocytes apoptosis was labeled by Annexin V-FITC/PI staining, and the protein expression of Bax and Bcl-2 were detected by immunohistochemisty staining in each group.
RESULTS AND CONCLUSION: The immunohistochemisty demonstrated that Bcl-2 expression in HP group was increased (P < 0.05), compared with control group, model group, and BMSCs group; While, compared with model group and BMSCs group, Bax expression in HP group was reduced, and the ratio of Bcl-2/Bax is maximum. Compared with control group and BMSCs group, cell viability in HP group was increased (P < 0.05), the apoptosis rate was reduced (P < 0.05). It suggested that HP may regulate Bax and Bcl-2 through the enhancement of paracrine mechanism, and which has a protective effect on cardiomyocytes apoptosis.

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