中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (38): 7082-7086.doi: 10.3969/j.issn.1673-8225.2010.38.013

• 药物控释材料 drug delivery materials • 上一篇    下一篇

微囊化HepG2细胞脂代谢与线粒体功能和蛋白的合成

肖  静1,2，张  英1，于炜婷1，郭  昕1，王  为1，马小军1　   

  1. 1中国科学院大连化学物理研究所生物医学材料工程组，辽宁省大连市 116023；2中国科学院研究生院，北京市 100039
  • 出版日期:2010-09-17 发布日期:2010-09-17
  • 通讯作者: 马小军，研究员，中国科学院大连化学物理研究所生物医学材料工程组，辽宁省大连市 116023 maxj@dicp.ac.cn
  • 作者简介:肖静☆，女，1980年生，新疆维吾尔自治区乌鲁木齐市人，汉族，中国科学院大连化学物理研究所在读博士，主要从事微囊化细胞培养研究。xiaoj@dicp.ac.cn
  • 基金资助:

    国家科学技术重大专项(2008ZX10002-019)“病毒性肝炎相关代谢紊乱的机制和用药指导研究”的子项目“肝癌体外三维药筛模型建立及评价”。国家自然科学基金资助项目(30970885)“细胞微囊化体系的热能/能量评价平台建立”。

Influence of altered lipid metabolism in microencapsulated HepG2 cells on the mitochondrial function and protein synthesis

Xiao Jing 1,2, Zhang Ying1, Yu Wei-ting1, Guo Xin1, Wang Wei1, Ma Xiao-jun1   

  1. 1 Laboratory of Biomedical Material Engineering, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian   116023, Liaoning Province, China; 2 Graduate School of the Chinese Academy of Sciences, Beijing   100039, China
  • Online:2010-09-17 Published:2010-09-17
  • Contact: Ma Xiao-jun, Investigator, Laboratory of Biomedical Material Engineering, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian 116023, Liaoning Province, China maxj@dicp.ac.cn
  • About author:Xiao Jing☆, Studying for doctorate, Laboratory of Biomedical Material Engineering, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian 116023, Liaoning Province, China; Graduate School of the Chinese Academy of Sciences, Beijing 100039, China xiaoj@dicp.ac.cn
  • Supported by:
    the National Natural Science Foundation of China, No. 30970885*; the National Science and Technology Major Project of China, No. 2008ZX10002-019*

PDF

451

被引次数

10

摘要：

背景：动、植物及微生物细胞在特殊微环境中培养时的生长与生产特性，与正常生理条件下或传统培养环境相比，具有明显变化，而这种变化是在不改变总体宏观环境与条件的前提下，实现了生物体微环境的相对有利。微囊微环境决定了细胞的生长和代谢行为，与微囊化细胞的功能息息相关。
目的：观察微囊化肝细胞脂代谢水平改变对细胞线粒体功能及蛋白合成能力的影响。
方法：将微囊化HepG2细胞接种于含1 μmol/L 氟伐他汀的MEM培养液中，在37 ℃，体积分数为5%CO2培养箱中培养。测定氟伐他汀干预前后微囊化HepG2细胞总胆固醇、三酰甘油、白蛋白水平变化以及线粒体功能变化。相差显微镜观察囊内细胞生长状态。
结果与结论：①微囊化HepG2细胞总胆固醇和三酰甘油水平随着培养时间延长显著增高(P < 0.05)；细胞线粒体功能出现抑制(P < 0.05)。②氟伐他汀能够降低囊内细胞总胆固醇水平(P < 0.05)，但对三酰甘油水平影响无显著差异(P > 0.05)。③氟伐他汀干预能在一定程度上缓解囊内出现的细胞线粒体功能抑制和白蛋白水平降低现象(P < 0.05)。结果提示微囊化细胞脂代谢水平变化尤其是胆固醇合成增加与细胞线粒体功能抑制及蛋白合成能力降低有关。

关键词: 微囊化细胞, 脂代谢, 线粒体, 蛋白合成, 氟伐他汀

Abstract:

BACKGROUND: The growth and production characteristics of animals, plants and microbial cells cultured in a special micro-environment, are different from those under normal physiological conditions or conventional culture environment, and this change achieves a relatively favorable micro-environment of the organisms under the premise of maintaining total macro-environment and conditions. Microencapsulated environment determines cell growth and metabolism behavior, and is closely related with function of microencapsulated cells.
OBJECTIVE: To study the influence of altered lipid metabolism occurred in microencapsulated hepatic cells on the mitochondrial function and protein synthesis capacity.
METHODS: Microencapsulated HepG2 cells were incubated in MEM with 1 μmol/L fluvastatin and cultured at 37 ℃ in an atmosphere with 5% volume fraction of CO2. The contents of total cholesterol, triglyceride, and albumin in the microencapsulated HepG2 cells were measured before and after fluvastatin intervention, as well as mitochondrial function. The growth of microencapsulated HepG2 cells was observed under phase-contrast microscopy.
RESULTS AND CONCLUSION: ①Total cholesterol and triglyceride were markedly increased in microencapsulated HepG2 cells with the increasing culture time (P < 0.05), and mitochondrial function declined (P < 0.05). ②Fluvastatin at 1 μmol/L reduced the total cholesterol levels in encapsulated HepG2 cells (P < 0.05), but there was no significant difference in the triglycerides level (P > 0.05). ③The inhibition of mitochondrial function and the reduction of albumin levels in microencapsulated cells can be relieved by fluvastatin (P < 0.05). Altered lipid metabolism in microencapsulated HepG2 cells, especially the increasing cholesterol synthesis, contributes to the mitochondrial function inhibition and protein synthesis decline.

中图分类号: