中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (20): 3703-3706.doi: 10.3969/j.issn.1673-8225.2012.20.021

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

改构型酸性成纤维细胞生长因子抑制新生大鼠心肌缺氧/复氧模型细胞的凋亡*★

李  彦1，王永玲1，李校堃2，李  菁3   

  1. 1新乡医学院病理生理学教研室，河南省新乡市 453003；2温州医学院生物与天然药物研究院，浙江省温州市325027；3暨南大学医学院病理生理学教研室，广东省广州市  510632
  • 收稿日期:2012-02-03 修回日期:2012-03-19 出版日期:2012-05-13 发布日期:2012-05-13
  • 通讯作者: 李菁，女，副研究员，硕士生导师，暨南大学医学院病理生理学教研室，广东省广州市 510632
  • 作者简介:李彦★，女， 1977年生，河南省南召县人，2005年暨南大学毕业，硕士，副教授，主要从事心肌缺血再灌注损伤方面的研究。 drleeyan@163.com
  • 基金资助:

    国家863计划资助项目(2002AA223318)。

Effect of modified acidic fibroblast growth factor against cardiomyocyte apoptosis in neonatal rats after anoxia/reoxygenation

Li Yan1, Wang Yong-ling1, Li Xiao-kun2, Li Jing3   

  1. 1Department of Pathophysiology, Xinxiang Medical University, Xinxiang  453003, Henan Province, China; 2Institute of Biology and Natural Medicines, Wenzhou Medical College, Wenzhou  325027, Zhejiang Province, China; 3Department of Pathophysiology, Jinan University Medical School, Guangzhou  510632, Guangdong Province, China
  • Received:2012-02-03 Revised:2012-03-19 Online:2012-05-13 Published:2012-05-13
  • Contact: Li Jing, Associate researcher, Master’s supervisor, Department of Pathophysiology, Jinan University Medical School, Guangzhou 510632, Guangdong Province, China
  • About author:Li Yan★, Master, Associate professor, Department of Pathophysiology, Xinxiang Medical University Medical school, Xinxiang 453003, Henan Province, China drleeyan@163.com
  • Supported by:

     the National 863 Program of China, No. 2002AA223318*

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摘要：

背景：酸性成纤维细胞生长因子对缺血及再灌注心肌具有较好的保护作用，删去N 端第21~27位的氨基酸序列后的改构型酸性成纤维细胞生长因子诱导的细胞增殖能力明显降低。
目的：观察改构型酸性成纤维细胞生长因子对心肌缺氧/复氧后细胞凋亡的影响。
方法：利用原代培养的SD新生大鼠心肌细胞建立体外心肌缺氧/复氧模型，分别用酸性成纤维细胞生长因子和改构型酸性成纤维细胞生长因子对此细胞模型进行干预。锥虫蓝拒染法检测心肌细胞存活率，流式细胞术检测心肌细胞凋亡率。
结果与结论：改构型酸性成纤维细胞生长因子及酸性成纤维细胞生长因子均能显著降低缺氧/复氧后心肌细胞存活率及凋亡率(P < 0.01)。证实，改构型酸性成纤维细胞生长因子能有效抑制缺氧/复氧后心肌细胞凋亡。
 

关键词:

酸性成纤维细胞生长因子, 心肌细胞, 缺氧, 复氧, 细胞凋亡, 组织构建

Abstract:

BACKGROUND: Acidic fibroblast growth factor (aFGF) can protect cardiomyocytes from ischemia/reperfusion damage, but the proliferative ability of the cells induced by modified aFGF (maFGF) is decreased.
OBJECTIVE: To study the effect of aFGF and maFGF on cardiomytes apoptosis after anoxia/reoxygenation.
METHODS: Myocardial anoxia/reoxygenation models with primary cultured cardiomyocytes from neonatal SD rats were established and then treated with aFGF and maFGF. The apoptosis rate of cardiomyocytes was detected by flow cytometry assay and the survival rate of cardiomyocytes was measured by typan blue exclusion.
RESULTS AND CONCLUSION: Pretreatment with aFGF and maFGF decreased the apoptosis rate of cardiomyocytes after anoxia/reoxygenation (P < 0.01). It has been proved that aFGF and maFGF have notable effects on attenuating cardiomyocyte apoptosis after anoxia/reoxygenation.

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