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|本期目录/Table of Contents|

饱和脂肪酸致乳鼠心肌细胞损伤凋亡的代谢机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第5期
页码:
652-656
栏目:
基础研究
出版日期:
2009-07-14

文章信息/Info

Title:
Metabolic mechanism of neonatal rat cardiomyocyte injury and apoptosis induced by saturated fatty acids
作者:
张治宇1; 赵彤1; 袁志忠2; 殷仁富2
第二军医大学：1.上海军职干休所，上海 200433，2.长征医院贵宾诊疗科，上海 200003
Author(s):
ZHANG Zhi-yu;  ZHAO Tong;  YUAN Zhi-zhong;  YIN Ren-fu
Sanatorium for Shanghai Army Retired Cadres, Second Military Medical University, Shanghai 200003, China
关键词:
鼠心肌细胞; FAT/CD36; 饱和脂肪酸; 细胞凋亡
Keywords:
rat cardiomyocyte;  FAT/CD36;  saturated fatty acid;  cell apoptosis
分类号:
Q547
DOI:
-
文献标识码:
A
摘要:
目的: 观察饱和脂肪酸所致乳鼠心肌细胞损伤凋亡过程中对脂肪酸摄取、利用的改变。方法: 应用饱和脂肪酸棕榈酸盐（palmitate，PMT）培养乳鼠心肌细胞，观察心肌细胞损伤、凋亡程度随时间的变化和心肌细胞发生凋亡前脂肪酸转运体（FAT/CD36）的表达、分布及肉碱脂酰基转移酶-1（CPT-1）活性的变化。结果: PMT诱导心肌细胞凋亡呈显著的时间依赖效应。与PMT共孵育4 h后，乳鼠心肌细胞膜中FAT/CD36的含量显著增加，且在时间上早于FAT/CD36 mRNA表达量的升高。在PMT处理早期，M-CPT-1 mRNA的表达量升高，并伴有CPT-1酶活性增强。随着与PMT共孵育时间的延长，心肌细胞膜FAT/CD36蛋白的含量未出现变化，但CPT-1酶的活性逐渐下降，心肌细胞凋亡的数量增加。结论: 心肌细胞对长链脂肪酸的摄取没有减少，但氧化利用能力下降，这可能为导致长链脂肪酸及其中间代谢产物在细胞内蓄积，损伤心肌细胞，引起心肌细胞凋亡的机制之一。
Abstract:
AIM: To study the changes of fatty acid uptake and utilization during saturated fatty acid-induced cardiomyocyte apoptosis in neonatal rats. METHODS: We observed palmitate-inducing cell apoptosis using annexin V-FITC and PI double-stained flow cytometry, change of fatty acid transporter/CD36 (FAT/CD36) expression and distribution using Western blotting, and activity of carnitine palmityl transferase-1 (CPT-1) using liquid scintillation detecting system. RESULTS: Cardiomyocyte apoptosis rate was increased significantly after 16 h treatment of palmitate. FAT/CD36 protein content on membrane increased significantly after 4 h treatment, whereas its mRNA increased significantly after 8 h treatment. Following the time of treatment by prolonged palmitate, there was no significant change of FAT/CD36 protein content on the membrane, but there was a significant decline of CPT-1 activity and increase of cardiomyocyte apoptosis. CONCLUSION: Accumulation of long-chain fatty acids and its intermediate metabolite in cardiomyocytes due to the decline of oxidation activity may be one of the mechanisms for palmitate-induced cardiomyocyte injury and apoptosis.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2008-12-15.基金项目：上海长征医院“三重三优”基金项目资助 通讯作者：殷仁富，教授，主要从事老年心脏病研究Email：yinrenfu28@sohu.com 作者简介：张治宇，主治医师，博士Email：zhang1978zy@hotmail.com
更新日期/Last Update: 2009-07-22