期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 476, 期 -, 页码 27-36出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2018.04.006
关键词
CTRP3; Cardiac dysfunction; Lipopolysaccharide; Sepsis; Inflammation; Apoptosis
资金
- Key Project of the National Natural Science Foundation [81530012]
- National Natural Science Foundation of China [81470516, 81270303]
C1q/tumor necrosis factor-related protein-3 (CTRP3) shows striking homologies of genomic structure to the adiponectin. In this study, we aimed to investigate the protective role of CTRP3 against sepsis-induced cardiomyopathy. Here, we overexpressed CTRP3 in myocardium by direct intramyocardial injection and constructed a model of lipopolysaccharide (LPS)-induced sepsis in mice. Our results demonstrated that cardiac-specific overexpression of CTRP3 remarkably attenuated myocardial dysfunction and increased the phosphorylation level of AMPK alpha during LPS-induced sepsis. The anti-inflammatory effects of CTRP3, as determined by decreased mRNA levels of TNF-alpha, IL-6 and a lower protein expression of phosphorylated NF-kappa B p65 and I kappa B alpha, was detected in mice following LPS treatment. Additionally, CTRP3 suppressed cardiac apoptosis induced by LPS in mice as indicated by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining and western blot for Cleaved-caspase3, Box and Bcl-2. In conclusion, CTRP3 could protect against sepsis-induced myocardial dysfunction in mice. The cardioprotective effects of CTRP3 might be mediated by activating AMPK alpha signaling pathway and blunting inflammatory response and apoptosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据