Induction of nuclear factor κB but not κB-responsive cytokine expression during myocardial reperfusion injury after neutropenia
Induction of nuclear factor κB but not κB-responsive cytokine expression during myocardial reperfusion injury after neutropenia
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DOI：
10.1016/s0891-5849(00)00273-2
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发表时间：
2000-06-01
影响因子：
7.4
通讯作者：
Freeman, GL
中科院分区：
文献类型：
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作者：
Chandrasekar, B;Colston, JT;Freeman, GL
中性粒细胞可能通过产生活性氧中间体（ROI）而导致心肌缺血/再灌注（I/R）损伤。 ROI 激活核因子 (NF)-kappa B，它调节具有负性肌力作用的细胞因子基因（白细胞介素 [IL]-1 beta、IL-6 和肿瘤坏死因子 [TNF]-alpha）。我们研究了中性粒细胞耗竭对 NF-kappa B DNA 结合活性以及心肌 IIR 损伤期间这些细胞因子表达的影响。雄性 WKY 大鼠 (n = 28) 接受单剂量抗中性粒细胞抗血清 (i/v)。 22小时后，当外周血中性粒细胞计数显着下降（减少94%）时，对动物进行15分钟的左冠状动脉前降支结扎，然后再灌注0.25、0.5、1、2、3和6小时（n = 4/组）。盐水处理的动物经历了类似的方案，并作为对照（n = 28，4/组）。中性粒细胞积累（由髓过氧化物酶活性定义）存在于对照中，但在抗 PMN 抗血清处理的动物中不存在（至少 p
Neutrophils may contribute to myocardial ischemia/reperfusion (I/R) injury by generating reactive oxygen intermediates (ROIs). ROIs activate nuclear factor (NF)-kappa B, which regulates genes for cytokines with negative inotropic effects (interleukin [IL]-1 beta, IL-6, and tumor necrosis factor [TNF]-alpha). We investigated the impact of neutrophil depletion on NF-kappa B DNA binding activity, and expression of these cytokines during myocardial IIR injury. Male WKY rats (n = 28) received a single dose of antineutrophil antiserum (i/v). Twenty two hours later, when the peripheral blood neutrophil counts were profoundly decreased (94% reduction), the animals underwent 15 min of left anterior descending coronary artery ligation followed by reperfusion for 0.25, 0.5, 1, 2, 3, and 6 h (n = 4/group). Saline-treated animals underwent a similar protocol, and served as controls (n = 28, 4/group). Neutrophil accumulation, defined by myeloperoxidase activity, was present in controls, but not in anti-PMN antisera-treated animals (at least p