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首页> 外文期刊>Translational Stroke Research >Bipyridine, an Iron Chelator, Does Not Lessen Intracerebral Iron-Induced Damage or Improve Outcome After Intracerebral Hemorrhagic Stroke in Rats
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Bipyridine, an Iron Chelator, Does Not Lessen Intracerebral Iron-Induced Damage or Improve Outcome After Intracerebral Hemorrhagic Stroke in Rats

机译：铁螯合剂联吡啶不能减轻大鼠脑出血引起的脑内铁诱导的损伤或改善结果

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摘要

Iron chelators, such as the intracellular ferrous chelator 2,2′-bipyridine, are a potential means of ameliorating iron-induced injury after intracerebral hemorrhage (ICH). We evaluated bipyridine against the collagenase and whole-blood ICH models and a simplified model of iron-induced damage involving a striatal injection of FeCl2 in adult rats. First, we assessed whether bipyridine (25 mg/kg beginning 12 h post-ICH and every 12 h for 3 days) would attenuate non-heme iron levels in the brain and lessen behavioral impairments (neurological deficit scale, corner turn test, and horizontal ladder) 7 days after collagenase-induced ICH. Second, we evaluated bipyridine (20 mg/kg beginning 6 h post-ICH and then every 24 h) on edema 3 days after collagenase infusion. Body temperature was continually recorded in a subset of these rats beginning 24 h prior to ICH until euthanasia. Third, bipyridine was administered (as per experiment 2) after whole-blood infusion to examine tissue loss, neuronal degeneration, and behavioral impairments at 7 days post-stroke, as well as body temperature for 3 days post-stroke. Finally, we evaluated whether bipyridine (25 mg/kg given 2 h prior to surgery and then every 12 h for 3 days) lessens tissue loss, neuronal death, and behavioral deficits after striatal FeCl2 injection. Bipyridine caused a significant hypothermic effect (maximum drop to 34.6 °C for 2–5 h after each injection) in both ICH models; however, in all experiments bipyridine-treated rats were indistinguishable from vehicle controls on all other measures (e.g., tissue loss, behavioral impairments, etc.). These results do not support the use of bipyridine against ICH.
机译：铁螯合剂，例如细胞内亚铁螯合剂2,2'-联吡啶，是缓解脑出血（ICH）后铁诱导的损伤的一种潜在手段。我们评估了联吡啶对胶原酶和全血ICH模型以及成年大鼠中纹状体注射FeCl2的铁引起的损伤的简化模型。首先，我们评估联吡啶（ICH后12小时开始，每12小时3天为25 mg / kg）是否会减弱大脑中的非血红素铁水平并减轻行为障碍（神经功能缺损量表，转弯试验和水平阶梯）在胶原酶诱导的ICH后7天。其次，我们在胶原酶注入后3天评估了双吡啶（ICH后6小时开始，然后每24小时20 mg / kg）。从ICH发生前24小时直到安乐死为止，连续记录这些大鼠的亚组的体温。第三，在全血输注后给予联吡啶（根据实验2），以检查中风后7天的组织损失，神经元变性和行为障碍，以及中风后3天的体温。最后，我们评估联吡啶（手术前2小时给予25 mg / kg，然后每12小时给予3天）减少纹状FeCl2注射后的组织损失，神经元死亡和行为缺陷。在两个ICH模型中，联吡啶引起了显着的低温效应（每次注射后2-5小时内最大降温至34.6°C）；但是，在所有实验中，联吡啶处理的大鼠在所有其他措施（例如组织损失，行为障碍等）上均与媒介物对照没有区别。这些结果不支持联吡啶用于ICH。

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