期刊文献+

高交感活性诱导的大鼠心肌损伤模型中氧化应激的受体调控机制 被引量:8

Dependence of adrenoceptor regulation on oxidative stress in cardiac injury induced by high sympathetic activity in rats
下载PDF
导出
摘要 目的:研究高交感活性诱发大鼠心肌损伤的氧化应激受体调控机制。方法:Sprague-Dawley(SD)大鼠随机分为对照组、模型组、普萘洛尔(Pro)组、哌唑嗪(Praz)组、普萘洛尔+哌唑嗪(Pro+Praz)组、维生素E(VE)组及普萘洛尔+哌唑嗪+维生素E(Pro+Praz+VE)组,除对照组外其余各组均腹腔注射去甲肾上腺素(NE)复制高交感活性引起的心肌损伤模型,同时灌胃给予相应药物,连续给药16 d,期间监测各组动物体重的变化。16 d后进行心室重构指标(心指数和羟脯氨酸含量)、病理组织学检查、氧化/抗氧化指标(MDA、SOD、CAT、GSH-Px和T-AOC)和能量代谢指标(Na+-K+ATPase和Ca2+-Mg2+ATPase)分析。结果:从第9天开始,模型组动物体重与对照组的比较差异有统计学意义(P<0.05),心指数和左心室肥厚明显增加,氧化/抗氧化和能量代谢障碍;Pro、Praz、Pro+Praz和VE各组均出现不同程度的动物体重、心指数、左心室肥厚和氧化/抗氧化失衡的改善;Pro、Praz和Pro+Praz能明显升高左心室Na+-K+ATPase和Ca2+-Mg2+ATPase的活性,Pro+Praz作用最明显(P<0.05)。结论:肾上腺素受体依赖是高交感活性诱导心肌氧化应激损伤的重要途径。 AIM:To investigate the dependence of the adrenoceptor regulation on oxidative stress in the rats with cardiac injury induced by high sympathetic activity .METHODS: Healthy SD rats were randomly divided into 7 groups:control, model, propranolol (Pro), prazosin (Praz), Pro+Praz, vitamin E (VE) and Pro+Praz+VE.The rats were intraperitoneally injected with norepinephrine ( NE) for continuous 16 d to reproduce cardiac injury , and treated with the respective drugs .During the experimental process , the body weight was recorded .At the end of the experiments , the following parameters were measured:the ventricular remodeling indexes ( cardiac index and hydroxyproline of the left ventricle), histopathologic examination , oxidative/antioxidative indexes [MDA, SOD, catalase (CAT), GSH-Px and total an-tioxidant capacity (T-AOC)], and energy metabolism (Na^+-K^+ATPase and Ca^2+-Mg^2+ATPase).RESULTS: The in-crease of body weight in model group was significantly slower than that in control group after 9 d of treatment (P〈0.05). The cardiac index and left ventricular hypertrophy were significantly increased .Oxidation/antioxidation and energy metabo-lism were disturbed.In Pro, Praz, Pro+Praz and VE groups, the body weight, cardiac index, left ventricular fibrosis and oxidative/antioxidative dysfunction were ameliorated .Pro, Praz and Pro +Praz increased the activity of Na ^+-K^+ATPase and Ca^2+-Mg^2+ATPase.Treatment with Pro+Praz showed the best result in all of the indexes (P〈0.05).CONCLU-SION:The dependence of adrenoceptor regulation plays an important role in the formation of oxidative stress in the process&amp;nbsp;of rat cardiac injury induced by high sympathetic activity .
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2014年第6期1029-1033,共5页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助项目(No.81173586) 教育部新世纪优秀人才支持计划(No.NCET-13-0747) 贵州省优秀科技教育省长专项资金资助项目(黔科教办[2011]28号) 贵州省社发攻关项目(黔科合SY字[2011]3011号) 贵州省科技厅科技攻关项目(黔科合SY字[2012]3085号)
关键词 高交感活性 氧化性应激 心肌损伤 High sympathetic activity Oxidative stress Cardiac injury
  • 相关文献

参考文献5

二级参考文献53

  • 1张小东,刘建文,李婷,曹艳,郭明川.胡黄连甙II和神经生长因子对H_2O_2损伤的PC12细胞的协同保护作用(英文)[J].中国临床药理学与治疗学,2007,12(1):32-37. 被引量:16
  • 2Peirce SM,Skalak TC,Rodeheaver GT.Ischemia-reperfusion injury in chronic pressure ulcer formation:a skin model in the rat.Wound Repair Regen,2000,8(1):68-76.
  • 3Reid RR,Sull AC,Mogford JE,et al.A novel murine model of cyclical cutaneous ischemia-reperfusion injury.J Surg Res,2004,116(1):172-180.
  • 4Salcido R,Fisher SB,Donofrio JC,et al.An animal model and computer-controlled surface pressure delivery system for the production of pressure ulcers.J Rehabil Res Dev,1995,32(2):149-161.
  • 5Sundin BM,Hussein MA,Glasofer S,et al.The role of allopurinol and deferoxamine in preventing pressure ulcers in pigs.Plast Reconstr Surg,2000,105(4):1408-1421.
  • 6Protasi F.Structural interaction between RYRs and DHPRs in calcium release units of cardiac and skeletal muscle cells.Front Biosci,2002,7:d650-658.
  • 7JEMAL A, BRAY F, CENTER M M, et al. Global cancer statistics[J]. CA Cancer J Clin, 2011, 61(2):69-90.
  • 8DE RAEDT T, WALTON Z, YECIES J L, et al. Exploiting cancer cell vulnerabilities to develop a combination therapy for ras-driven tumors[J]. Cancer Cell, 2011,20(3):400-413.
  • 9MAURO C, LEOW S C, ANSO E, et al. NF-kB controls energy homeostasis and metabolic adaptation by upregulating mitochondrial respiration[J]. Nat Cell Biol, 2011, 13(10):1272-1279.
  • 10HADZIC T, AYKIN-BURNS N, ZHU Y, et al. Paclitaxel combined with inhibitors of glucose and hydroperoxide metabolism enhances breast cancer cell killing via HzO2-mediated oxidative stress[J]. Free Radic Biol Med, 2010,48(8):1024-1033.

共引文献14

同被引文献81

  • 1闻立君,王金,陈景超,辛嫣琼,曲韵智.丹参配伍人参抗缺血性心脏病研究进展[J].黑龙江医药,2012,25(5):678-679. 被引量:7
  • 2中国高血压防治指南修订委员会.中国高血压防治指南[M].2010年修订版.北京:人民卫生出版社,2011:31-31.
  • 3刘会芳,赵燕燕.百草枯中毒机制及临床治疗现状与展望[J].中国急救医学,2007,27(11):1042-1044. 被引量:31
  • 4Lai RC, Arslan F, Lee MM, et al. Exosome secreted by MSC reduces myocardial ischemia/reperfusion injury[J].Stem Cell Res, 2010, 4(3):214-222.
  • 5Hu L, Zhou L, Wu X, et al. Hypoxic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury through AMPK/eNOS/PGC-1α signaling pathway[J].Int J Clin Exp Patho, 2014, 7(11): 7378-7388.
  • 6Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease[J].J Am Soc Nephrol, 2011, 22(1):124-136.
  • 7Zhao L, Peng DQ, Zhang J, et al. Extracellular signal-regulated kinase 1/2 activation is involved in intermedin 1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion[J].Peptides, 2012, 33(2):329-335.
  • 8Lim K, Lu TS, Molostvov G, et al. Vascular Klotho deficiency potentiates the development of human artery calcification and mediates resistance to fibroblast growth factor 23[J].Circulation, 2012, 125(18):2243-2255.
  • 9Doi S, Zou Y, Togao O, et al. Klotho inhibits transforming growth factor-β1 (TGF-β1) signaling and suppresses renal fibrosis and cancer metastasis in mice[J].J Biol Chem, 2011, 286(10):8655-8665.
  • 10Fukuda K, Asoh S, Ishikawa M, et al. Inhalation of hydrogen gas suppresses hepatic injury caused by ischemia/reperfusion through reducing oxidative stress[J].Biochem Biophys Res Commun, 2007, 361(3):670-674.

引证文献8

二级引证文献40

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部