Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats.
Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats.
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DOI：
10.1111/j.1582-4934.2007.00009.x
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发表时间：
2007-01
影响因子：
5.3
通讯作者：
Fineschi V
中科院分区：
文献类型：
--
作者：
Neri M;Cerretani D;Fiaschi AI;Laghi PF;Lazzerini PE;Maffione AB;Micheli L;Bruni G;Nencini C;Giorgi G;D'Errico S;Fiore C;Pomara C;Riezzo I;Turillazzi E;Fineschi V
背景：为了研究活性氧（ROS）和儿茶酚胺自动氧化产物的心脏毒性作用，我们研究了：（1）抗氧化心脏细胞防御系统对去甲肾上腺素（NE）给药诱导的氧化应激的反应，（2）通过受体结合测定来研究NE给药对心脏β1-肾上腺素能受体的影响，（3）与NE给药和细胞因子之间的生物串扰相关的细胞形态改变[肿瘤] [坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)、白细胞介素IL6、IL8、IL10]方法与结果：实验共使用195只雄性大鼠。所有动物在处死前均接受心电图（EKG）检查。结果表明，NE 给药会影响抗氧化细胞防御系统，显着增加谷胱甘肽过氧化物酶 (GPx)、谷胱甘肽还原酶 (GR) 和超氧化物歧化酶 (SOD) 的活性。氧化型谷胱甘肽（GSH/GSSG）比率显着降低，丙二醛（MDA）水平增加，显示心脏组织的脂质过氧化状态。我们描述了受损心肌中随机稀疏的显着细胞凋亡过程以及 ROS 对 NE 介导的 TNF-α、MCP-1 和 IL6、IL8、IL10 产生的影响。结论：我们的结果支持这样的假设：儿茶酚胺可能通过其自动氧化产生的反应中间体诱导氧化损伤，无论它们与肾上腺素能受体的相互作用如何，因此是儿茶酚胺诱导的心脏毒性发病机制的一个重要因素。心脏抑制性细胞因子的增加可以解释为受损心肌对注射NE引起的心脏功能障碍的适应性反应。
Background: To investigate the cardiotoxic role of reactive oxygen species (ROS) and of products derived from catecholamines auto-oxidation, we studied: (1) the response of antioxidant cardiac cellular defence systems to oxidative stress induced by norepinephrine (NE) administration, (2) the effect of NE administration on cardiac β1-adrenergic receptors by means of receptor binding assay, (3) the cellular morphological alterations related to the biologically cross-talk between the NE administration and cytokines [tumor necrosis factor-alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1), interleukins IL6, IL8, IL10]Methods and Results: A total of 195 male rats was used in the experiment. All animals underwent electrocardiogram (EKG) before being sacrificed. The results obtained show that NE administration influences the antioxidant cellular defence system significantly increasing glutathione peroxidase (GPx) activity, glutathione reductase (GR) and superoxide dismutase (SOD). The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue. We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-α, MCP-1, and IL6, IL8, IL10 production. Conclusions: Our results support the hypothesis that catecholamines may induce oxidative damage through reactive intermediates resulting from their auto-oxidation, irrespective of their interaction with adrenergic receptors, thus representing an important factor in the pathogenesis of catecholamines-induced cardiotoxicity. The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.
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