• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Nicotinamide therapy protects against both necrosis and apoptosis in a stroke model.
【24h】

Nicotinamide therapy protects against both necrosis and apoptosis in a stroke model.

机译：烟酰胺疗法可预防中风模型中的坏死和凋亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND AND PURPOSE: Nicotinamide protects against brain damage in ischemia-reperfusion. However, the dosage and time of treatment require clarification. It is also not clear if nicotinamide can protect against both necrosis and apoptosis. METHODS: Dose-response and time-effect studies were designed. Transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 min. Different doses of nicotinamide were injected upon reperfusion. In time-effect studies, 500 mg/kg nicotinamide was administered at different times after the onset of reperfusion. Neurological finding scores were recorded. Infarct volumes were measured. RESULTS: In contrast to controls, neurological deficit scores and infarct volumes were greatly reduced by treatment with nicotinamide. The ED(50) of nicotinamide was 239+/-79 mg/kg (P=.95). It was found that nicotinamide injected during the first 6 h of reperfusion could effectively inhibit the development of brain damage. The optimal dose of nicotinamide was 500 mg/kg and gave a maximal response. CONCLUSIONS: Poly(ADP-ribose) polymerase (PARP) plays a key role in DNA repair in stroke. Excessive PARP activity consumes NAD leading to energy depletion and neuronal damage. As an inhibitor of PARP, nicotinamide promotes the supply of energy. The results suggest that early application of nicotinamide at a suitable dosage significantly ameliorates necrotic and apoptotic brain injury after focal ischemia-reperfusion.
机译：背景与目的：烟酰胺可防止缺血再灌注中的脑损伤。但是，治疗的剂量和时间需要澄清。还不清楚烟酰胺是否能同时抵抗坏死和凋亡。方法：设计了剂量反应和时间效应研究。大脑中动脉阻塞（MCAO）诱导90分钟，引起短暂性局灶性脑缺血。再灌注后注射不同剂量的烟酰胺。在时间效应研究中，在再灌注开始后的不同时间施用500 mg / kg烟酰胺。记录神经学评分。测量梗死体积。结果：与对照组相比，烟酰胺治疗可大大减少神经功能缺损评分和梗塞体积。烟酰胺的ED（50）为239 +/- 79 mg / kg（P = .95）。研究发现，在再灌注的前6小时内注射烟酰胺可以有效抑制脑损伤的发展。烟酰胺的最佳剂量为500 mg / kg，可产生最大反应。结论：聚（ADP-核糖）聚合酶（PARP）在中风的DNA修复中起关键作用。 PARP过度活动会消耗NAD，从而导致能量消耗和神经元受损。烟酰胺作为PARP的抑制剂，可促进能量的供应。结果表明，以适当剂量早期使用烟酰胺可明显改善局灶性缺血再灌注后坏死性和凋亡性脑损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号