[棕榈酸诱导人肝癌细胞系HepG2细胞凋亡]
[Palmitic acid induces apoptosis in human hepatoma cell line, HepG2 cells].
作者信息
Zhang Li, Ji Jun, Zhu Xiao-Yu, Wu Yuan-Yuan, Yu Huan, Zhang Bin, Li Xue-Ling, Sun Xi-Zhuo
机构信息
Department of Central Laboratory, Dalian Municipal Central Hospital, Dalian University Medical College, Dalian 116033, China.
出版信息
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2004 Dec;26(6):671-6.
OBJECTIVE
To investigate the effects of palmitic acid (PA) on human hepatocytes and its mechanism.
METHODS
We administered a mimic hyperlipidemia condition of 0.2-0.4 mmol/L PA to human hepatoma cell line, HepG2 cells. Cell viability was determined by Trypan blue staining. Cell cycle and early apoptosis were determined by propidium iodide and/or Annexin V staining, and the levels of Bcl-2 and Bax were analyzed by flow cytometry.
RESULTS
An inhibition of cell growth was observed at a dose- and time-dependent manner in HepG2 cells after the treatment of PA. An apoptosis with appearance of sub-G1 fraction determined by cell cycle analysis significantly increased after the treatment of PA for 4 days. Bcl-2 level slightly decreased; in contrast, Bax level elevated markedly, which resulted in a significant decrease of Bcl-2/Bax ratio.
CONCLUSION
PA may induce cell death on hepatocytes via mitochondria-mediated apoptosis by reducing the level of Bcl-2/Bax.
目的
研究棕榈酸（PA）对人肝细胞的影响及其机制。
方法
我们将0.2 - 0.4 mmol/L PA模拟高脂血症条件应用于人肝癌细胞系HepG2细胞。通过台盼蓝染色测定细胞活力。通过碘化丙啶和/或膜联蛋白V染色测定细胞周期和早期凋亡，并通过流式细胞术分析Bcl-2和Bax的水平。
结果
PA处理后，HepG2细胞中观察到细胞生长呈剂量和时间依赖性抑制。PA处理4天后，通过细胞周期分析确定的亚G1期凋亡显著增加。Bcl-2水平略有下降；相反，Bax水平显著升高，导致Bcl-2/Bax比值显著降低。
结论
PA可能通过降低Bcl-2/Bax水平，经由线粒体介导的凋亡诱导肝细胞死亡。
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