Three pentacyclic triterpenes protect H9c2 cardiomyoblast cells against high-glucose-induced injury

被引:30
作者
Chan, C. Y. [1 ]
Mong, M. C. [2 ]
Liu, W. H. [3 ]
Huang, C. Y. [1 ]
Yin, M. C. [1 ,2 ]
机构
[1] China Med Univ, Dept Nutr, Taichung, Taiwan
[2] Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung, Taiwan
[3] Chung Shan Med Univ, Dept Nutr, Taichung, Taiwan
关键词
H9c2; cell; asiatic acid; boswellic acid; ROS; NF-kB; INDUCED DIABETIC-RATS; OXIDATIVE STRESS; OLEANOLIC ACID; URSOLIC ACID; ASIATIC ACID; MICE; CARDIOMYOPATHY; HYPERGLYCEMIA; ACTIVATION; APOPTOSIS;
D O I
10.3109/10715762.2014.880113
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
H9c2 cardiomyoblast cell line was used to examine the protection of three triterpenes, asiatic acid, boswellic acid, and oleanolic acid, at 5 or 10 mu M against high-glucose-induced injury. High glucose stimulated reactive oxygen species (ROS), oxidized glutathione (GSSG), interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 production, as well as decreased glutathione peroxidase (GPX), glutathione reductase (GR) and catalase activities, and protein expression. However, pre-treatments of three triterpenes reserved glutathione, maintained activity and expression of GPX, GR, and catalase, as well as lowered ROS, GSSG, and inflammatory cytokines generation. High glucose reduced Na+ -K+ -ATPase activity, raised nuclear factor kappa (NF-kappa) B and caspase-3 activities, up-regulated protein expression of NF-kappa. B, mitogen-activated protein kinase, Bax, and cleaved caspase-3, as well as down-regulated Bcl-2 expression. Pre-treatments of three triterpenes retained Na+ -K+ -ATPase activity, declined NF-kappa B and caspase-3 activities, reserved Bcl-2 expression, as well as suppressed protein expression of NF-kappa B, p-p38, Bax, and cleaved caspase-3. These findings suggest that these triterpenes are potent cardiac-protective agents.
引用
收藏
页码:402 / 411
页数:10
相关论文
共 32 条
  • [1] Diabetic cardiomyopathy: Insights into pathogenesis, diagnostic challenges, and therapeutic options
    Aneja, Ashish
    Tang, W. H. Wilson
    Bansilal, Sameer
    Garcia, Mario J.
    Farkouh, Michael E.
    [J]. AMERICAN JOURNAL OF MEDICINE, 2008, 121 (09) : 748 - 757
  • [2] Hyperglycemia-induced apoptosis in mouse myocardium -: Mitochondrial cytochrome c-mediated caspase-3 activation pathway
    Cai, L
    Li, W
    Wang, GW
    Guo, LP
    Jiang, YC
    Kang, YJ
    [J]. DIABETES, 2002, 51 (06) : 1938 - 1948
  • [3] Anti-inflammatory and anti-coagulatory activities of caffeic acid and ellagic acid in cardiac tissue of diabetic mice
    Chao, Pei-chun
    Hsu, Cheng-chin
    Yin, Mei-chin
    [J]. NUTRITION & METABOLISM, 2009, 6
  • [4] Rote of endothelin-1, sodium hydrogen exchanger-1 and mitogen activated protein kinase (MAPK) activation in glucose-induced cardiomyocyte hypertrophy
    Chen, Shali
    Khan, Zia A.
    Karmazyn, Morris
    Chakrabarti, Subrata
    [J]. DIABETES-METABOLISM RESEARCH AND REVIEWS, 2007, 23 (05) : 356 - 367
  • [5] Antiinflammatory and antiatherogenic effects of the NF-κB inhibitor acetyl-11-keto-β-boswellic acid in LPS-challenged ApoE-/- mice
    Cuaz-Perolin, Clarisse
    Billiet, Ludivine
    Bauge, Eric
    Copin, Corinne
    Scott-Algara, Daniel
    Genze, Felicitas
    Buechele, Berhold
    Syrovets, Tatiana
    Simmet, Thomas
    Rouis, Mustapha
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2008, 28 (02) : 272 - 277
  • [6] Dhalla NS, 2012, EXP CLIN CARDIOL, V17, P115
  • [7] Drimal Jan, 2008, Endocr Regul, V42, P129
  • [8] Oxidative Stress and Diabetic Complications
    Giacco, Ferdinando
    Brownlee, Michael
    [J]. CIRCULATION RESEARCH, 2010, 107 (09) : 1058 - 1070
  • [9] Oxidative stress in heart failure - More than just damage
    Grieve, DJ
    Shah, AM
    [J]. EUROPEAN HEART JOURNAL, 2003, 24 (24) : 2161 - 2163
  • [10] Possible pathophysiology of heart failure in obesity: Cardiac apoptosis
    Huang, Chih-Yang
    Lee, Shin-Da
    [J]. BIOMEDICINE-TAIWAN, 2012, 2 (01): : 36 - 40