软脂酸诱导人肝癌HepG2细胞的凋亡  

Palmitic Acid Induces Apoptosis in Human Hepatoma Cell Line,HepG2 Cells

作　　者：张利[1] 纪军[1] 朱晓钰[1] 吴园园[1] 于环[1] 张槟[1] 李雪岭[1] 孙喜琢[1] 

机构地区：[1]大连大学医学院附属大连市中心医院中心实验室,大连116033

出　　处：《中国医学科学院学报》2004年第6期671-676,共6页Acta Academiae Medicinae Sinicae

摘　　要：目的探讨软脂酸(PA)对肝细胞的损害作用及其机制。方法采用人肝癌细胞系HepG2细胞为研究对象,观察PA对细胞生存力的影响。用Trypanblue法检测细胞死亡率;流式细胞记数仪检测细胞周期;AnnexinⅤ和碘化丙啶双重染色定量检测早期凋亡及Bcl-2/Bax的表达。结果在人HepG2细胞系中PA诱导了时间相关性细胞死亡和剂量依赖性的细胞生存能力下降;PA诱导了HepG2细胞随处理时间而增加的早期凋亡,PA处理后HepG2细胞中Bcl-2/Bax的比值下降。结论PA能诱导肝细胞凋亡,其机制可能与下调Bcl-2/Bax比值有关。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.

关 键 词：软脂酸 肝癌细胞 细胞凋亡 

分 类 号：R575.5[医药卫生—消化系统]