• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >TNFalpha is required to confer protection in an in vivo model of classical ischaemic preconditioning.
【24h】

TNFalpha is required to confer protection in an in vivo model of classical ischaemic preconditioning.

机译：在经典的缺血预处理的体内模型中，需要提供TNFalpha保护。

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

Although Tumor Necrosis Factor alpha (TNFalpha) is used as a preconditioning mimetic in vitro, its role in ischaemic preconditioning (IPC) has not been clearly defined. Here, we propose to use an in vivo model (that takes into account the activation of leukocytes which may affect levels of TNFalpha) to demonstrate that i) TNFalpha acts as a trigger in IPC and ii) the dose-dependent nature of this cardioprotective effect of TNFalpha. Male Wistar rats were subjected to 30 min of left coronary artery occlusion (index ischaemia), followed by 24 h reperfusion. In the presence or absence of a soluble TNFalpha receptor (sTNFalpha-R), preconditioning was induced by 3 cycles of ischaemia (3 min)/reperfusion (5 min) (IPC) or various doses (0.05-4 microg/kg) of exogenous TNFalpha. Following 24 h reperfusion, infarct size (IS, expressed as % of the area at risk (AAR)) was assessed. Tissue levels of TNFalpha from the AAR, following IPC and TNFalpha stimulus were determined using Western Blot. IPC caused decrease inIS (4.5+/-1.3% vs 30.8+/-4.3% in ischaemic rats; P<0.001) and increase of TNFalpha levels following the IPC stimulus. The protective effect of IPC was abrogated in the presence of the sTNFalpha-R. In addition, exogenous TNFalpha dose-dependently reduced IS with maximal protection at a dose of 0.1 microg/kg (IS=12.6%, P<0.01 vs ischaemic). In conclusion our data provide strong evidence for a role of TNFalpha during the trigger phase of IPC. In addition, exogenous TNFalpha mimics IPC by providing a dose-dependent cardioprotective effect against ischaemia-reperfusion injury in vivo.
机译：尽管肿瘤坏死因子α（TNFalpha）在体外用作模拟预处理，但尚不清楚其在缺血预处理（IPC）中的作用。在这里，我们建议使用体内模型（考虑到白细胞的激活可能影响TNFalpha的水平）来证明i）TNFalpha在IPC中起触发作用; ii）这种心脏保护作用的剂量依赖性TNFalpha。对雄性Wistar大鼠进行30分钟的左冠状动脉闭塞（指数缺血），然后再灌注24 h。在存在或不存在可溶性TNFalpha受体（sTNFalpha-R）的情况下，通过3次局部缺血（3分钟）/再灌注（5分钟）（IPC）或各种剂量（0.05-4 microg / kg）的外源性诱导预处理TNFα。再灌注24小时后，评估梗死面积（IS，以危险区域（AAR）的百分比表示）。使用Western Blot测定IPC和TNFalpha刺激后来自AAR的TNFalpha的组织水平。在IPC刺激后，IPC导致IS降低（缺血大鼠的IS降低（4.5 +/- 1.3％，而30.8 +/- 4.3％; P <0.001））和TNFα水平升高。在sTNFalpha-R的存在下，IPC的保护作用被取消。此外，外源性TNFα剂量依赖性地降低IS，并以0.1 microg / kg的剂量提供最大保护（IS = 12.6％，与缺血相比，P <0.01）。总之，我们的数据为TNFalpha在IPC触发阶段的作用提供了有力的证据。另外，外源性TNFα通过提供针对体内缺血-再灌注损伤的剂量依赖性心脏保护作用来模仿IPC。

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