全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
-  2018 

抑制CD36过表达减轻糖尿病大鼠心肌缺血/再灌注损伤 Inhibition of CD36 Overexpression Attenuates Myocardial Ischemia-Reperfusion Injury in Diabetic Rats

Keywords: 糖尿病,心肌缺血/再灌注损伤,FAT/CD36,磺基-N-琥珀酰亚胺酯油酸

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的:探讨抑制CD36过表达在糖尿病大鼠心肌缺血/再灌注损伤中的作用和机制。方法:成年雄性健康大鼠,体重210-240g。大鼠糖尿病模型采取腹腔注射1%链脲佐菌素60mg/kg制备。大鼠冠状动脉左前降支分结扎30min后再灌注2h来制备心肌缺血/再灌注模型。正常大鼠和造模成功的糖尿病大鼠被分为3组(n=16):非糖尿病心肌缺血/再灌注组(IR组)、糖尿病心肌缺血/再灌注组(DIR组),CD36的抑制剂SSO处理的糖尿病心肌缺血/再灌注组(DIRS组)。再灌注结束,获取心肌组织和血样本。Western Blot法检测心肌CD36表达,TTC法检测心肌梗死面积,HE染色观察心肌组织病理变化,检测血糖,血清中胰岛素、甘油三酯(TGs)和游离脂肪酸(FFAs)。检测血清15-F2t-isoprostane、LDH、CK-MB及BNP。结果:DIR组的心肌CD36表达明显高于IR组而低于DIRS组(P<0.05),DIRS组的心肌缺血面积和梗死面积均减少(P<0.05);DIR和DIRS组糖尿病大鼠的胰岛素、TGs和FFAs的浓度均高于非糖尿病大鼠IR组(P<0.05),SSO处理的大鼠血清中胰岛素、TGs和FFAs的浓度均有不同程度下降(P<0.05)。DIR组的15-F2t-isoprostane、LDH、CK-MB和BNP浓度均高于IR组(P<0.05),而经SSO处理后,DIRS组这些指标的浓度均有所下降(P<0.05)。结论:SSO部分抑制CD36过表达,减轻了糖尿病大鼠心肌缺血/再灌注损伤

References

[1]  Mansor LS,Sousa FM,Yea G,et al.Inhibition of sarcolemmal FAT/CD36 by sulfo-N-succinimidyl oleate rapidly corrects metabolism and restores function in the diabetic heart following hypoxia/reoxygenation[J].Cardiovasc Res,2017,113(7):737-748.
[2]  Lopaschuk GD,Ussher JR,Folmes CD,et al.Myocardial fatty acid metabolism in health and disease[J].Physiol Rev,2010,90(1):207-258.
[3]  Kuda O,Pietka TA,Demianova Z,et al.Sulfo-N-succinimidyl oleate(SSO)inhibits fatty acid uptake and signaling for intracellular calcium via binding CD36lysine 164:SSO also inhibits oxidized low density lipoprotein uptake by macrophages[J].J Biol Chem,2013,288(22):15 547-15 555.
[4]  Danaei G,Singh GM,Paciorek CJ,et al.The global cardiovascular risk transition:associations of four metabolic risk factors with national income,urbanization,and Western diet in 1980and 2008[J].Circulation,2013,127(14):1 493-1 502,1 501e-1 502e.
[5]  Abumrad NA,El-Maghrabi MR,Amri EZ,et al.Cloning of a rat adipocyte membrane protein implicated in binding or transport of long-chain fatty acids that is induced during preadipocyte differentiation.Homology with human CD36[J].J Biol Chem,1993,268(24):17 665-17 668.
[6]  Kim TT,Dyck JR.The role of CD36in the regulation of myocardial lipid metabolism[J].Biochim Biophys Acta,2016,1 861(10):1 450-1 460.
[7]  Fukushima A,Lopaschuk GD.Cardiac fatty acid oxidation in heart failure associated with obesity and diabetes[J].Biochim Biophys Acta,2016,1 861(10):1 525-1 534.
[8]  Glatz JF,Nabben M,Heather LC,et al.Regulation of the subcellular trafficking of CD36,a major determinant of cardiac fatty acid utilization[J].Biochim Biophys Acta,2016,1 861(10):1 461-1 471.
[9]  Naville D,Duchampt A,Vigier M,et al.Link between intestinal CD36ligand binding and satiety induced by a high protein diet in mice[J].PLoS One,2012,7(1):e30686.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133