%0 Journal Article
%T Salusin-汕 contributes to oxidative stress and inflammation in diabetic cardiomyopathy
%A Bing Zhou
%A Feng Zhang
%A Guo-Qing Zhu
%A Li Ling
%A Ming-Xia Zhao
%A Qi Chen
%A Xiao-Qing Xiong
%A Yu-Ming Kang
%A Yue-Hua Li
%J Archive of "Cell Death & Disease".
%D 2017
%R 10.1038/cddis.2017.106
%X Salusin-汕 accelerates inflammatory responses in vascular endothelial cells, and increases oxidative stress in vascular smooth muscle cells. Plasma salusin-汕 levels were increased in diabetic patients. This study was designed to determine whether salusin-汕 is involved in the pathogenesis of diabetic cardiomyopathy (DCM), and whether knockdown of salusin-汕 attenuates cardiac inflammation and oxidative stress in rats with DCM. H9c2 or neonatal rat cardiomyocytes were incubated with 33.3ˋmM of glucose to mimic the high glucose (HG) in diabetes. Streptozotocin and high-fat diet were used to induce type 2 diabetes in rats. HG induced salusin-汕 expression in H9c2 cells. Salusin-汕 caused greater responses of oxidative stress, NF百B activation and inflammation in HG-treated H9c2 cells than these in control H9c2 cells. Diphenyleneiodonium (a NAD(P)H oxidase inhibitor) or N-acetylcysteine (an antioxidant) inhibited the salusin-汕-induced NF百B activation and inflammation. Bay11-7082 (a NF百B inhibitor) attenuated salusin-汕-induced inflammation but not oxidative stress. Knockdown of salusin-汕 prevented the HG-induced oxidative stress, NF百B activation and inflammation in neonatal rat cardiomyocytes. Silencing salusin-汕 with adenoviruse-mediated shRNA had no significant effects on blood glucose and insulin resistance, but attenuated ventricular dysfunction in diabetic rats. Oxidative stress, NF百B activation, inflammation, salusin-汕 upregulation in myocardium of diabetic rats were prevented by knockdown of salusin-汕. These results indicate that salusin-汕 contributes to inflammation in DCM via NOX2/ROS/NF百B signaling, and that knockdown of salusin-汕 attenuates cardiac dysfunction, oxidative stress and inflammation in DCM
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386515/