Changes in the Expression of MIF and Other Key Enzymes of Energy Metabolism in the Myocardia of Broiler Chickens with Ascites Syndrome

腹水综合征肉鸡心肌MIF等能量代谢关键酶表达的变化

阅读:6
作者:Lifang Li, Qiufeng Jia, Lingli Chen, Wenkui Wang

Abstract

Ascites syndrome (AS) is a metabolic disease observed mainly in fast-growing broilers. The heart is one of the most important target organs of the disease. The goal of this study was to evaluate the metabolic function of the right ventricles in clinical ascitic broilers. HE staining was performed to observe histopathological changes in the right ventricle of the heart, while Western blotting was used to detect the protein expression levels of macrophage migration inhibitory factor (MIF) and phosphorylated AMP-activated protein kinase (p-AMPK), as well as other key enzymes of energy metabolic pathways (i.e., glycolytic pathway: HK2, PFK1, PFK2, and PKM2; the tricarboxylic acid cycle (TCA cycle) pathway: OGDH, IDH2, and CS; and the fatty acid oxidation pathway: CPT-1A and ACC) in myocardial tissue. The histopathological examination of the myocardia of ascitic broilers revealed disoriented myocardial cells in the myofibril structure and a large number of blood cells deposited in the intermyofibrillar vessels, suggesting right heart failure in ascitic broilers. The Western blotting analysis demonstrated significantly increased levels of MIF and p-AMPK in the myocardia of ascitic broilers compared to those of the control group (p < 0.05). Additionally, the protein expression of key enzymes was dramatically increased in the glycolytic and fatty acid oxidation pathways, while the protein expression of key enzymes in the TCA cycle pathway was decreased in the ascitic broiler group. These findings suggest enhanced glycolysis and fatty acid oxidation metabolism, and a diminished TCA cycle, in the myocardia of broiler chickens with ascites syndrome.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。