中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (2): 252-256.doi: 10.3969/j.issn.1673-8225.2012.02.014

• 骨组织构建 • 上一篇    下一篇

肝细胞生长因子对急性失代偿性心力衰竭模型小鼠的保护

段  伟1，李  力2，刘新宾2，张红超2
  

  1. 1河北北方学院，河北省张家口市  075000； 2解放军空军总医院心血管外科，北京市 100142
  • 收稿日期:2011-11-10 修回日期:2011-11-21 出版日期:2012-01-08 发布日期:2012-01-08
  • 通讯作者: 张红超，博士后，副主任医师，解放军空军总医院心血管外科，北京市 100142 zhanghc2002@ gmail.com
  • 作者简介:段伟★，男，1981年生，河北省石家庄市人，汉族，河北北方学院在读硕士，医师，主要从事生物因子对心力衰竭的保护作用的研究。 andy-duan@ 163.com
  • 基金资助:

    国家自然科学基金项目 ：针对(30872539)IL-6 用基因干扰(RNAi)技术逆转心肌细胞信号通路改变。

Protective effect of hepatocyte growth factor in model mice of acute decompensated heart failure

 Duan Wei1  , Li Li2 , Liu Xin-bin2  , Zhang Hong-chao2   

  1. 1Hebei North University, Zhangjiakou  075000, Hebei Province, China;
    2Department of Cardiothoracic Surgery, Air Force General Hospital of Chinese PLA, Beijing  100142, China 
     
  • Received:2011-11-10 Revised:2011-11-21 Online:2012-01-08 Published:2012-01-08
  • Contact: Zhang Hong-chao, Doctor, Associate chief physician, Department of Cardiothoracic Surgery, Air Force General Hospital of Chinese PLA, Beijing 100142, China zhanghc2002@ gmail.com
  • About author:Duan Wei,★ Studying for master’s degree, Physician, Hebei North University, Zhangjiakou 075000, Hebei Province, China andy-duan@163.com
  • Supported by:
    the National Natural Science Foundation of China, No. 30872539*  

PDF

450

被引次数

4

摘要：

背景：肝细胞生长因子是一种心肌营养因子，具有很强的抑制心肌细胞凋亡与心室重构，促血管内皮细胞有丝分裂作用。
目的：观察肝细胞生长因子对急性失代偿性心力衰竭模型小鼠的保护作用。
方法：将50只昆明小鼠随机分为5组：正常对照组、慢性心力衰竭组、急性失代偿性心力衰竭组、慢性心力衰竭治疗组、急性失代偿性心力衰竭治疗组。采用尾静脉注射阿霉素建立慢性心力衰竭小鼠模型，第7周尾静脉注射细菌脂多糖制作急性失代偿性心力衰竭模型，随后慢性心力衰竭治疗组、急性失代偿性心力衰竭治疗组同时给予尾静脉注射肝细胞生长因子干预。
结果与结论：与慢性心力衰竭组比较，慢性心力衰竭治疗组心室壁厚度、左室射血分数值明显增加，白细胞介素6减少，脑钠肽下降，Bax蛋白表达减少，Bcl-2蛋白表达增加，心肌细胞凋亡明显减少(P < 0.01或0.05)。与急性失代偿性心力衰竭组比较，急性失代偿性心力衰竭治疗组心室壁厚度、左室射血分数值明显增加，脑钠肽表达下调，白细胞介素6明显下降，Bcl-2蛋白表达增加，Bax蛋白表达减少(P < 0.01或0.05)。说明肝细胞生长因子通过抗炎性因子作用，抗心肌细胞凋亡作用明显改善急性失代偿性心力衰竭小鼠的心脏功能。

关键词: 肝细胞生长因子, 慢性心力衰竭, 急性失代偿性心力衰竭, 内毒素, 阿霉素

Abstract:

BACKGROUND: Hepatocyte growth factor is a kind of myocardial nutritional factors. It has a strong inhibitory effect on myocardial apoptosis and ventricular remodeling. Meanwhile, it promotes the mitosis of vascular endothelial cells.
OBJECTIVE: To explore the protective effect of hepatocyte growth factor on model mice of acute decompensated heart failure.
METHODS: A total of 50 Kunming mice were randomly divided into five groups: normal control group, chronic heart failure group, acute decompensated heart failure group, chronic heart failure treated group and acute decompensated heart failure treated group. Chronic heart failure model in mice was constructed using tail intravenous injection of adriamycin. Mice in the corresponding group were intravenously injected with bacterial lipopolysaccharide through tail vein to construct acute decompensated heart failure model. Mice in the chronic heart failure treated group and acute decompensated heart failure treated group were intravenously injected with hepatocyte growth factor through tail vein.  
RESULTS AND CONCLUSION:Compared with chronic heart failure group, the thickness of ventricles and left ventricular ejection fraction in the chronic heart failure treated group increased significantly; the content of interleukin-6 and brain natriuretic peptide decreased; the expression of Bax protein decreased while the expression of Bcl-2 protein increased; the myocardial apoptosis reduced significantly (  < 0.01 or  < 0.05). Compared with acute decompensated heart failure group, the thickness of ventricles P P and left ventricular ejection fraction in the acute decompensated heart failure treated group increased significantly; the content of brain natriuretic peptide decreased while the content of interleukin-6 decreased significantly; the expression of Bax protein decreased while the expression of Bcl-2 protein increased (  < 0.01 or   < 0.05). These findings indicate that hepatocyte growth P Pfactor significantly improve the heart function of acute decompensated heart failure mice by anti-inflammatory effect and resisting cardiac muscle cell apoptosis.

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