中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (15): 2741-2744.doi: 10.3969/j.issn.1673-8225.2012.15.018

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

肝细胞生长因子在肿瘤坏死因子相关凋亡诱导配体作用下对原代肝星状细胞增殖及凋亡的影响**☆

张君红，姜海行，覃山羽，陆正峰，孟云超，宁  琳，杨  文   

  1. 广西医科大学第一附属医院消化内科，广西壮族自治区南宁市   530021
  • 收稿日期:2011-09-16 修回日期:2011-10-29 出版日期:2012-04-08 发布日期:2012-04-08
  • 通讯作者: 姜海行，教授，博士生导师，广西医科大学第一附属医院消化内科，广西壮族自治区南宁市 530021 jihaxi@163.com
  • 作者简介:张君红☆，女，1972年生，广西壮族自治区桂林市人，汉族，广西医科大学在读博士，主治医师，主要从事干细胞在肝损伤修复机制中作用的研究。 junjun12162001@163.com
  • 基金资助:

    广西自然科学基金资助项目(0897008)；广西壮族自治区卫生厅自筹经费科研课题(Z2011317)。

Effect of hepatocyte growth factor on the proliferation and apoptosis of primary hepatic stellate cells under tumor necrosis factor-related apoptosis-inducing ligand

Zhang Jun-hong, Jiang Hai-xing, Qin Shan-yu, Lu Zheng-feng, Meng Yun-chao, Ning Lin, Yang Wen   

  1. Department of Gastroenterology, the First Affiliated Hospital of Guangxi Medical University, Nanning  530021, Guangxi Zhuang Autonomous Region, China
  • Received:2011-09-16 Revised:2011-10-29 Online:2012-04-08 Published:2012-04-08
  • Contact: author: Jiang Hai-xing, Professor, Doctoral supervisor, Department of Gastroenterology, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China jihaxi@163.com
  • About author:Zhang Jun-hong☆, Studying for doctorate, Attending physician, Department of Gastroenterology, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China junjun12162001@163.com
  • Supported by:

    the Natural Science Foundation of Guangxi, No. 0897008*; Self-funded Research Projects, Health Department of Guangxi Zhuang Autonomous Region, No. Z2011317*  

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244

被引次数

3

摘要：

背景：活化的肝星状细胞是肝纤维化的关键因素，研究表明肝细胞生长因子能促进星状细胞凋亡，其具体机制可能与增强肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导星状细胞凋亡有关。
目的：观察肿瘤坏死因子相关凋亡诱导配体作用下，肝细胞生长因子对原代肝星状细胞增殖、凋亡的影响并初步探讨其可能机制。
方法：将SD大鼠原代肝星状细胞复苏、传代，细胞增殖明显时用于实验。实验分为4组：空白对照组为单纯肝星状细胞培养；肝细胞生长因子组：将100 μg/L肝细胞生长因子作用于肝星状细胞；TRAIL组：将2 mg/L的TRAIL作用于肝星状细胞；肝细胞生长因子+TRAIL组：将肝细胞生长因子预先刺激肝星状细胞24 h，再加入2 mg/L TRAIL。
结果与结论：MTT检测显示肝细胞生长因子及TRAIL分别在50~200 μg/L、0.5~1.5 mg/L各浓度下对肝星状细胞增殖抑制率无影响，TRAIL在2 mg/L作用下对肝星状细胞有抑制作用。流式细胞仪检测肝细胞生长因子+TRAIL组的中晚期凋亡率明显高于空白对照组及肝细胞生长因子组(P < 0.05)；肝细胞生长因子+TRAIL组DR5荧光强度明显高于其他3组(P < 0.01)。提示在TRAIL作用下，肝细胞生长因子能促进肝星状细胞的凋亡、抑制其增殖。可能与肝细胞生长因子上调活化肝星状细胞表面DR5表达有关。
 

关键词: 肝星状细胞, 肿瘤坏死因子相关凋亡诱导配体, 肝细胞生长因子, 凋亡, 死亡受体5

Abstract:

BACKGROUND: Activated hepatic stellate cells play a key role in liver fibrosis. Research shows that hepatocyte growth factor (HGF) can promote the apoptosis of activated hepatic stellate cells and the specific mechanisms may have relationship with the apoptosis of enhanced-related apoptosis-inducing ligand (TRAIL)-induced stellate cells.
OBJECTIVE: To investigate the role of HGF under the action of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in primary hepatic stellate cells (HSCs) proliferation, apoptosis and to explore the possible mechanisms involved.
METHODS: Primary HSCs of SD rats were used to recovery and passage, and were used in the experiment when the proliferation was obvious. HSCs were divided into four groups: ① blank control group, HSCs cultured alone; ② HGF group,    100 μg/L HGF was injected into HSCs; ③ TRAIL group, 2 mg/L TRAIL was injected into HSCs; ④ HGF+TRAIL group, the HSCs were prestimulated by HGF for 24 hours and then 2 mg/L TRAIL was injected into HSCs.
RESULTS AND CONCLUSION: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that HGF at 50- 200 μg/L and TRAIL at 0.5-1.5 mg/L had no effect on HSCs proliferation. 2 mg/L rate TRAIL could inhibit HSCs proliferation. Mid and late apoptosis of HSCs was detected by flow cytometry, the apoptosis rate in the HGF+TRAIL group was higher than that in the blank control group and the HGF group (P < 0.05); the DR5 fluorescence intensity in the HGF+TRAIL group was higher than that in the blank control group, the HGF group and the TRAIL group (P < 0.01). Under the action of the TRAIL, HGF could promote the apoptosis of HSCs and inhibit the proliferation. The possible machanism was that HGF could increase the expression of DR5 on HSCs surface.
Zhang JH, Jiang HX, Qin SY, Lu ZF, Meng YC, Ning L, Yang W. Effect of hepatocyte growth factor on the proliferation and apoptosis of primary hepatic stellate cells under tumor necrosis factor-related apoptosis-inducing ligand. Zhongguo Zuzhi Gongcheng Yanjiu. 2012;16(15): 2741-2744.     [http://www.crter.cn  http://en.zglckf.com]

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