• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion.
【24h】

Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion.

机译：抑制p38可减轻小鼠的心肌梗塞损伤，但不能减轻缺血再灌注后的猪的心肌梗塞损伤。

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

The MAPK family member p38 is activated in the heart after ischemia-reperfusion (I/R) injury. However, the cardioprotective vs. proapoptotic effects associated with p38 activation in the heart after I/R injury remain unresolved. Another issue to consider is that the majority of past studies have employed the rodent as a model for assessing p38's role in cardiac injury vs. protection, while the potential regulatory role in a large animal model is even more uncertain. Here we performed a parallel study in the mouse and pig to directly compare the extent of cardiac injury after I/R at baseline or with the selective p38 inhibitor SB-239063. Infusion of SB-239063 5 min before ischemia in the mouse prevented ischemia-induced p38 activation, resulting in a 25% reduction of infarct size compared with vehicle-treated animals (27.9 +/- 2.9% vs. 37.5 +/- 2.7%). In the pig, SB-239063 similarly inhibited myocardial p38 activation, but there was no corresponding effect on the degree of infarction injury (43.6 +/- 4.0% vs. 41.4 +/- 4.3%). These data suggest a difference in myocardial responsiveness to I/R between the small animal mouse model and the large animal pig model, such that p38 activation in the mouse contributes to acute cellular injury and death, while the same activation in pig has no causative effect on these parameters.
机译：MAPK家族成员p38在缺血/再灌注（I / R）损伤后在心脏中被激活。但是，与I / R损伤后心脏中p38激活相关的心脏保护作用与促凋亡作用仍未得到解决。另一个要考虑的问题是，过去的大多数研究已将啮齿动物用作评估p38在心脏损伤与保护作用中的作用的模型，而在大型动物模型中潜在的调节作用甚至还不确定。在这里，我们在小鼠和猪中进行了一项平行研究，以直接比较基线I / R或选择性p38抑制剂SB-239063后的心脏损伤程度。小鼠缺血前5分钟输注SB-239063可阻止缺血诱导的p38活化，与溶媒治疗的动物相比，梗死面积减少25％（27.9 +/- 2.9％比37.5 +/- 2.7％） 。在猪中，SB-239063同样抑制了心肌p38的活化，但是对梗死程度没有相应的影响（43.6 +/- 4.0％对41.4 +/- 4.3％）。这些数据表明，小动物小鼠模型和大动物猪模型之间的心肌对I / R的反应性有所不同，因此小鼠中的p38激活可导致急性细胞损伤和死亡，而猪中的相同激活则没有致病作用在这些参数上。

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