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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*
引用本文:王羿,柏帅,徐旖旎,江滟,陶玲,刘兴德,沈祥春. 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*[J]. 中国病理生理杂志, 2014, 30(6): 1029-1033. DOI: 10.3969/j.issn.1000-4718.2014.06.012
作者姓名:王羿  柏帅  徐旖旎  江滟  陶玲  刘兴德  沈祥春
作者单位:贵阳医学院 1药理研究室, 2附属医院心内科,贵州 贵阳 550004
基金项目: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)
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。

关 键 词:高交感活性  氧化性应激  心肌损伤  
收稿时间:2013-12-30

Dependence of adrenoceptor regulation on oxidative stress in cardiac injury induced by high sympathetic activity in rats
WANG Yi,BAI Shuai,XU Yi-ni,JIANG Yan,TAO Ling,LIU Xing-de,SHEN Xiang-chun. Dependence of adrenoceptor regulation on oxidative stress in cardiac injury induced by high sympathetic activity in rats[J]. Chinese Journal of Pathophysiology, 2014, 30(6): 1029-1033. DOI: 10.3969/j.issn.1000-4718.2014.06.012
Authors:WANG Yi  BAI Shuai  XU Yi-ni  JIANG Yan  TAO Ling  LIU Xing-de  SHEN Xiang-chun
Affiliation:1Research Division of Pharmacology, 2Department of Cardiology, Affiliated Hospital, Guiyang Medical University, Guiyang 550004, China.
Abstract: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 antioxidant capacity (T-AOC)], and energy metabolism (Na+-K+ ATPase and Ca2+-Mg2+ATPase). RESULTS:The increase 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 metabolism 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 Ca2+-Mg2+ATPase. Treatment with Pro+Praz showed the best result in all of the indexes (P<0.05). CONCLUSION:The dependence of adrenoceptor regulation plays an important role in the formation of oxidative stress in the process of rat cardiac injury induced by high sympathetic activity.
Keywords:High sympathetic activity  Oxidative stress  Cardiac injury
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