我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

脂联素通过增强线粒体生物合成和功能减轻高糖/高脂诱导的心肌细胞损伤

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2013年第2期
页码:
146-150
栏目:
基础研究
出版日期:
2013-04-25

文章信息/Info

Title:
Adiponectin exerts cardioprotective effects against high-glucose/high-fat-induced injury of neonatal rat cardiomyocytes through increasing mitochondrial biogenesis and function
作者:
王 瀚闫文俊周 芬张立剑李文婷刘佩林陶 凌
(第四军医大学西京医院心内科,陕西 西安 710032)
Author(s):
WANG Han YAN Wen-jun ZHOU Fen ZHANG Li-jian LI Wen-ting LIU Pei-lin TAO Ling
(Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
脂联素心肌细胞高糖/高脂线粒体生物合成线粒体功能
Keywords:
adiponectin cardiomyocytes high-glucose/high-fat mitochondrial biogenesis mitochondrial function
分类号:
R589.2
DOI:
-
文献标识码:
A
摘要:
目的:观察脂联素(APN)是否通过增强线粒体生物合成和功能减轻高糖/高脂所致心肌细胞损伤。方法: 分离培养SD乳鼠的心肌细胞,培养3 d后分为3组:即对照组(培养基中含5 mmol/L葡萄糖和20 mmol/L甘露醇)、高糖/高脂组(培养基中含25 mmol/L葡萄糖和500 μmol/L软脂酸钠,培养18 h)及高糖/高脂+APN组(培养基中含25 mmol/L葡萄糖,500 μmol/L软脂酸钠和3 μg/ml APN球状片段,培养18 h)。高糖/高脂处理后,检测转录因子Tfam mRNA的水平、细胞线粒体膜电位与心肌细胞的凋亡。结果: 与对照组比较,高糖/高脂组Tfam mRNA的水平与线粒体膜电位均降低,细胞凋亡增加;APN处理可逆转上述作用。结论: 高糖/高脂降低心肌线粒体生物合成和导致线粒体功能障碍;APN可通过增加线粒体的生物合成和功能而发挥对心肌保护的作用。
Abstract:
AIM:To investigate whether adiponectin (APN) generates cardioprotection in response to high-glucose/high-fat damage through increasing mitochondrial biogenesis and functions. METHODS: Cultured neonatal rat ventricular myocytes (NRVM) were randomized into control group (5 mmol/L glucose and 20 mmol/L mannitol), high-glucose/high-fat group (25 mmol/L glucose and 500 μmol/L sodium palmitate, 18 h incubation) and high-glucose/high-fat+APN group (25 mmol/L glucose, 500 μmol/L sodium palmitate and 3 μg/ml globular APN, 18 h incubation) after 3 days of normal culture. Cells were harvested for evaluation of mitochondrial membrane potential and mRNA levels of Tfam after high-glucose/high-fat incubation. RESULTS: Compared with those in control group, both mitochondrial membrane potential and mRNA levels of Tfam decreased and cell apoptosis increased in high-glucose/high-fat group. However, these changes were reversed by APN. CONCLUSION: High-glucose/high-fat can lead to mitochondrial dysfunction in cardiomyocytes and APN can protect cardiomyocytes by increasing mitochondrial biogenesis and functions.

参考文献/References

[1]Petersen KF,Dufour S,Befroy D,et al.Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes[J].N Engl J Med,2004,350(7):664-671.
[2]Pischon T,Girman CJ,Hotamisligil GS,et al.Plasma adiponectin levels and risk of myocardial infarction in men[J].JAMA,2004,291(14):1730-1737.
[3]Palanivel R,Fang X,Park M,et al.Globular and full-length forms of adiponectin mediate specific changes in glucose and fatty acid uptake and metabolism in cardiomyocytes[J].Cardiovasc Res,2007,75(1):148-157.
[4]Goldstein BJ,Scalia R.Adipokines and vascular disease in diabetes[J].Curr Diab Rep,2007,7(1):25-33.
[5]Hotta K,Funahashi T,Arita Y,et al.Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients[J].Arterioscler Thromb Vasc Biol,2000,20(6):1595-1599.
[6]Kumada M, Kihara S, Sumitsuji S, et al. Association of hypoadiponectinemia with coronary artery disease in men[J].Arterioscler Thromb Vasc Biol,2003,23(1):85-89.
[7]Kuo TH,Moore KH,Giacomelli F,et al.Defective oxidative metabolism of heart mitochondria from genetically diabetic mice[J].Diabetes, 1983,32(9):781-787.
[8]Kuo TH,Giacomelli F,Wiener J.Oxidative metabolism of Polytron versus Nagarse mitochondria in hearts of genetically diabetic mice[J].Biochim Biophys Acta,1985,806(1):9-15.
[9]Bugger H,Abel ED.Mitochondria in the diabetic heart[J].Cardiovasc Res,2010, 88(2):229-240.
[10]Peterson LR,Herrero P,Schechtman KB,et al.Effect of obesity and insulin resistance on myocardial substrate metabolism and effici-ency in young women[J].Circulation,2004,109(18):2191-2196.
[11]Anderson EJ,Kypson A P,Rodriguez E,et al.Substrate-specific derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart[J].J Am Coll Cardiol,2009,54(20):1891-1898.
[12]Joseph AM, Joanisse DR,Baillot RG,et al.Mitochondrial dysregulation in the pathogenesis of diabetes: potential for mitochondrial biogenesis-mediated interventions[J].Exp Diabetes Res,2012,2012:642038.
[13]Scarpulla RC.Transcriptional paradigms in mammalian mitochondrial biogenesis and function[J].Physiol Rev,2008,88(2):611-638.
[14]Parisi MA,Clayton DA.Similarity of human mitochondrial transcription factor 1 to high mobility group proteins[J].Science,1991,252(5008):965-969.
[15]Dong F,Li Q,Sreejayan N,et al.Metallothionein prevents high-fat diet induced cardiac contractile dysfunction:role of peroxisome proliferator activated receptor gamma coactivator 1alpha and mitochondrial biogenesis[J].Diabetes,2007,56(9):2201-2212.
[16]Sparagna GC,Hickson-Bick DL,Buja LM,et al.A metabolic role for mitochondria in palmitate-induced cardiac myocyte apoptosis[J].Am J Physiol Heart Circ Physiol,2000,279(5):H2124-H2132.
[17]Iwabu M,Yamauchi T,Okada-Iwabu M,et al.Adiponectin and AdipoR1 regulate PGC-1alpha and mitochondria by Ca(2+) and AMPK/SIRT1[J].Nature,2010,464(7293):1313-1319.
[18]Zhou M,Xu A,Tam PK,et al.Mitochondrial dysfunction contributes to the increased vulnerabilities of adiponectin knockout mice to liver injury[J]. Hepatology, 2008, 48(4):1087-1096.
[19]Shibata R, Sato K, Pimentel DR,et al.Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms[J].Nat Med,2005,11(10):1096-1103.
[20]Tao L,Gao E,Jiao X,et al.Adiponectin cardioprotection after myocardial ischemia/reperfusion involves the reduction of oxidative/nitrative stress[J].Circulation,2007,115(11):1408-1416.

备注/Memo

备注/Memo:
收稿日期:2012-11-03.基金资助:国家自然科学基金项目资助(81170186,81225001) 通讯作者:陶凌,主任医师,主要从事糖尿病心肌缺血/再灌注损伤的研究 Email:lingtao2006@gmail.com 作者简介:王瀚,硕士生 Email:harry19870921@126.com
更新日期/Last Update: 2013-04-28