Salusin-β contributes to oxidative stress and inflammation in diabetic cardiomyopathy

• DOI: 10.1038/cddis.2017.106
• Publication Date: 2017-03-23T13:57:16Z
• Authors: Ming-Xia Zhao; Bing Zhou; Li Ling; Xiao-Qing Xiong; Feng Zhang; Qi Chen; Yue-Hua Li; Yu-Ming Kang; Guo-Qing Zhu
• Keywords: Diabetic Cardiomyopathy

Salusin-β accelerates inflammatory responses in vascular endothelial cells, and increases oxidative stress smooth muscle cells. Plasma salusin-β levels were increased diabetic patients. This study was designed to determine whether is involved the pathogenesis of cardiomyopathy (DCM), knockdown attenuates cardiac inflammation rats with DCM. H9c2 or neonatal rat cardiomyocytes incubated 33.3 mM glucose mimic high (HG) diabetes. Streptozotocin high-fat diet used induce type 2 diabetes rats. HG induced expression caused greater stress, NFκB activation HG-treated cells than these control Diphenyleneiodonium (a NAD(P)H oxidase inhibitor) N-acetylcysteine (an antioxidant) inhibited salusin-β-induced inflammation. Bay11-7082 attenuated but not stress. Knockdown prevented HG-induced cardiomyocytes. Silencing adenoviruse-mediated shRNA had no significant effects on blood insulin resistance, ventricular dysfunction Oxidative activation, inflammation, upregulation myocardium by salusin-β. These results indicate that contributes DCM via NOX2/ROS/NFκB signaling, dysfunction,