Neri Margherita, Fineschi Vittorio, Di Paolo Marco, Pomara Cristoforo, Riezzo Irene, Turillazzi Emanuela, Cerretani Daniela
Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
Curr Vasc Pharmacol. 2015;13(1):26-36. doi: 10.2174/15701611113119990003.
Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protection. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-α (Tumor Necrosis Factor α), IL-1β (Interleukin- 1β) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.
心力衰竭或缺血/再灌注期间的氧化应激是自由基或其氧化产物过度生成或积累的结果。氧化应激期间形成的自由基可引发脂质过氧化，将蛋白质氧化为失活状态并导致DNA链断裂。氧化应激是一种由于氧化剂代谢产物生成增加或细胞保护机制改变而产生毒性作用的状态。在急性心脏缺血的早期阶段，细胞因子具有功能多效性和冗余性的特点，此外，几种细胞因子对同一细胞类型发挥相似和重叠的作用，一种细胞因子对多种细胞类型表现出广泛的生物学效应。众多研究证实梗死心肌中细胞因子级联反应被激活。在心肌梗死的实验模型中，不断有关于促炎细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）以及趋化因子的诱导和释放的描述。本综述探讨急性心肌梗死后氧化应激和促炎细胞因子反应的作用，并探究心脏损伤的炎症机制。
