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Emodin-mediated protection from acute myocardial infarction via inhibition of inflammation and apoptosis in local ischemic myocardium

机译:大黄素介导的通过抑制局部缺血心肌的炎症和细胞凋亡来预防急性心肌梗死

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摘要

Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. in a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappa B activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis. (c) 2007 Published by Elsevier Inc.
机译:急性心肌梗死(AMI)与炎症和细胞凋亡相关。大黄素在几种炎性疾病中起抗炎作用。最近的研究表明,大黄素可以预防心肌缺血/再灌注损伤。然而,其作用基础的机制仍然未知。在AMI小鼠模型中,基于左冠状动脉的结扎,大黄素的给药以剂量依赖性方式降低了心肌梗塞面积(MIS)。大黄素显着抑制局部心肌梗塞区域的TNF-α表达和NF-κB活化。大黄素的治疗通过抑制caspase-3激活来抑制心肌细胞凋亡。因此,这些研究表明大黄素通过抑制局部炎症和细胞凋亡来保护心肌细胞免受损伤。 (c)2007年由Elsevier Inc.发布。

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