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|本期目录/Table of Contents|

磷酸肌酸对心肌细胞线粒体的保护作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第1期
页码:
14-16
栏目:
实验研究
出版日期:
2004-01-01

文章信息/Info

Title:
Protective effect of phosphocreatine on mitochondrial membrane in cardiomyocytes
作者:
刘瑛琪1;  李天德2;  任艺虹2;  李宁3
1.解放军306医院心内科, 北京 100101; 解放军总医院: 2.心内科, 3.仪器中心, 北京 100853
Author(s):
LIU Ying-qi1;  LI Tian-de2;  REN Yi-hong2;  LI Ning3
1.Cardiology Department of 306 Hospital of PLA, Beijing 100101
关键词:
线粒体膜电位; 磷酸肌酸; 细胞凋亡
Keywords:
mitochondrial membrane potential;  phosphocreatine;  apoptosis
分类号:
R541.6
DOI:
-
文献标识码:
A
摘要:
目的:研究能量治疗对心力衰竭的治疗机制。观察磷酸肌酸(phosphocreatine, CP)对心肌细胞线粒体膜电位的保护作用。方法:采用胶原酶分离成年大鼠心肌细胞,0.2 mmol/L H2O2刺激细胞,于刺激前10 min加入10 mmol/L CP,利用荧光探针JC-1结合流式细胞仪检测线粒体膜电位的变化;AnnexinV/PI及TUNEL染色法鉴定心肌细胞的凋亡。结果:H2O2导致线粒体膜电位下降,细胞凋亡增加。CP有效地减低了线粒体膜电位的下降,减少了细胞凋亡。结论:CP能够抗心肌细胞氧化损伤,其机制可能依赖于减少或抑制线粒体膜电位的下降,保护了线粒体的正常功能。
Abstract:
AIM: To observe the protective effect of phosphocreatine on mitochondrial function in rat cardiomyocytes. METHODS: Using H2O2 to cause oxidative stress, CP was given tenmintes before H2O2 stimulation. JC-1 in combination with flow cytometry was used to measre the changes of mitochondrial membrane potential. Apoptosis was identified by means of double florescence staining with Annexin V-FITC/propidim iodide and TUNEL staining. RESULTS: H2O2 caused the decrease of mitochondrial membrane potential and the increase of apoptosis rate. But in the CP treatment group, mitochondrial membrane potential wasn't decreased significantly. CONCLUSON: CP can prevent the cardiomyocyte from oxidatie injry. The mechanism may rely on inhiiting the decrease of mitochondrial membrane potential and protecting mitochondrial function.

参考文献/References

[1]Suzuki S, Kostin S, Person V, et al. Time course of the apoptotic cascade and effects of caspase inhibitors in adult rat ventricular cardiomyocytes[J]. J Mol Cell Cardiol, 2001, 33: 983-994.

[2]Semenovsky ML, Shumakov VI, Sharov VG, et al. Protection of ischemic myocardium by exogenous phosphocreatine[J]. J Thorac Cardiovasc Surg, 1984, 87: 190-200.

[3]Glick R, Burns H, Reddy J, et al. Dispersion and isolation of beating cells from adult rat heart[J]. Anal Bioche, 1974, 61: 32-42.

[4]Halestrap AP, Kerr PM, Javadov S, et al. Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion inury of the heart[J]. Biohs Acta, 1998, 1366: 79-94.

[5]Mathur A, Hong Y, Kemp BK, et al. Evaluation of fluorescent dyes for the detection of mitochondrial membrane potential changes in cultured cardiomyocytes[J]. Cardiovasc Res, 2000, 46: 126-138.

[6]Dwn WH, Chasseaud LF, Ballard SA, et al. The effect of intravenously administered phosphocreatine on ATP and phosphocreatine concentrations in the cardiac muscle of the rat [J]. Drug Res, 1983, 33(1): 552-554.

[7]Jacobus WE. Respiratory control and the integration of heart high-energy phosphate metablism by mitochondrial creatine kinase[J]. Ann Rev Phsiol, 1985, 47: 707-725.

备注/Memo

备注/Memo:
收稿日期：2003-2-6.
更新日期/Last Update: 2004-01-01