常建华,景桂霞,党旭云 磷酸肌酸预处理对糖尿病大鼠心肌缺血再灌注损伤的保护作用及其机制 |
论文编辑部-新丝路理论网 2011-03-31 15:19:52 作者:中华医学之家:http://www.xinxi85.com 来源: 文字大小:[大][中][小] |
|
Title:
The protective effect of phosphocreatine preconditioning on myocardial ischemia-reperfusion injury in diabetic rats and its action mechanisms
- 文章编号:
- 1671-8259(2011)02-0151-04
- 作者:
- 常建华; 景桂霞; 党旭云
- 西安交通大学医学院第一附属医院麻醉科,陕西西安 710061
- Author(s):
- CHANG Jian-hua; JING Gui-xia; DANG Xu-yun
- Department of Anesthesiology, the First Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710061, China
- 关键词:
- ; 磷酸肌酸; 糖尿病大鼠; 心肌缺血再灌注损伤; 线粒体; 凋亡
- Keywords:
- ; phosphocreatine; diabetic rat; myocardium ischemia-reperfusion injury; mitochondrion; apoptosis
- 分类号:
- R587.1
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 摘要:目的 探讨磷酸肌酸(PCr)预处理对糖尿病大鼠心肌缺血再灌注损伤的保护作用及其机制。方法 诱导糖尿病大鼠模型,2周后随机分为3组:假手术组(D1),缺血再灌注组(D2),缺血再灌注+PCr给药组(D3);观察缺血区心肌线粒体超微结构,计算凋亡指数(AI),测定心肌匀浆中磷酸腺苷和PCr的含量,并计算能荷值(EC)。结果 与D2组相比,D3组线粒体肿胀变性的损伤较轻,AI降低,ATP、PCr含量和EC均升高(P<0.05)。结论 PCr通过维护心肌线粒体结构和功能的完整性,提高心肌组织内能量物质的含量,减少心肌细胞的凋亡,从而对糖尿病大鼠心肌缺血再灌注损伤起到保护作用。
- Abstract:
- ABSTRACT: Objective To investigate the protective effect of phosphocreatine (PCr) preconditioning on myocardial ischemia-reperfusion injury in diabetic rats and its action mechanisms. Methods A diabetic rat model was induced first; two weeks later these rats were divided randomly into 3 groups: sham-operation group (D1), myocardial ischemia-reperfusion group (D2) and ischemia reperfusion + PCr preconditioning group (D3). The ultrastructure of the cardiac muscle and mitochondria was observed under an electron microscope, the content of high-energy compounds in the cardiac muscle and apoptosis index (AI) were measured, and the value of energy charge (EC) was calculated. Results Compared with those in D2, the mitochondria damage was alleviated, AI decreased while adenosine triphosphate (ATP), PCr content and EC increased in D3 (P<0.05). Conclusion PCr can protect mitochondrial structure and function, enhance the content of high-energy compounds in the myocardial cells and reduce myocardial apoptosis, thus fighting against myocardial ischemia-reperfusion injury in diabetic rats.
参考文献/References
[1]VINOKUR V, LEIBOWITZ G, GRINBERG L, et al. Diabetes and the heart: could the diabetic myocardium be protected by preconditioning [J]? Redox Rep, 2007, 12(6):246-256. [2]KATAKAM PV, JORDAN JE, SNIPES JA, et al. Myocardial preconditioning against ischemia-reperfusion injury is abolished in Zucker obese rats with insulin resistance [J]. Am J Physiol Regul Integr Comp Physiol, 2007, 292 (2):R920-926. [3]刘瑛琪,任艺虹,李天德,等. 磷酸肌酸保护心肌细胞线粒体功能机制初探 [J]. 军医进修学院学报, 2004, 25(1):15-17. [4]侯立向. 一种心肌保护剂:磷酸肌酸 [J]. 生物化学与生物物理进展, 2003, 30(2):324. [5]TAHA M, LOPASCHUK GD. Alterations in energy metabolism in cardiomyopathies [J]. Ann Med, 2007, 39(8):594-607. [6]LAZAR HL. Alterations in myocardial metabolism in the diabetic myocardium [J]. Semin Thorac Cardiovasc Surg, 2006, 18(4):289-292. [7]ZHAO G, JEOUNG NH, BURGESS SC, et al. Overexpression of pyruvate dehydrogenase kinase 4 in heart perturbs metabolism and exacerbates calcineurin-induced cardiomyopathy [J]. Am J Physiol Heart Circ Physiol, 2008, 294(2):936-943. [8]PETERSON LR, HERRERO P, MCGILL J, et al. Fatty acids and insulin modulate myocardial substrate metabolism in humans with type 1 diabetes [J]. Diabetes, 2008, 57(1):32-40. [9]BRIEDE J, STIVRINA M, VIGANTE B, et al. Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heart [J]. Cell Biochem Funct, 2008, 26(2):238-245. [10]ROSANO GM, VITALE C, FRAGASSO G. Metabolic therapy for patients with diabetes mellitus and coronary artery disease [J]. Am J Cardiol, 2006, 98(5A):14J-18J.
中华医学之家:http://www.xinxi85.com
投稿信箱:zhyxzj85@163.com
联系电话:029--85327298 主编QQ:693891972 |
|
|
|
|