Resveratrol ameliorates myocardial fibrosis by inhibiting ROS/ERK/TGF-β/periostin pathway in STZ-induced diabetic mice

• DOI: 10.1186/s12872-015-0169-z
• Publication Date: 2016-01-11T00:14:28Z
• Authors: Han Wu; Guan-Nan Li; Jun Xie; Ran Li; Qin-Hua Chen; Jian-Zhou Chen; Zhong-Hai Wei; Li-Na Kang; Biao Xu
• Keywords: Periostin; Myofibroblast; Cardiac Fibrosis; Diabetic Cardiomyopathy; Myocardial fibrosis

Myocardial fibrosis is an essential hallmark of diabetic cardiomyopathy (DCM) contributing to cardiac dysfunctions. Resveratrol, antioxidant, exerts its anti-fibrotic effect via inhibition oxidative stress, while the underlying molecular mechanism remains largely elusive. Periostin, a fibrogenesis matricellular protein, has been shown be associated with stress. In present study, we investigated role periostin in resveratrol streptozocin (STZ)-induced heart and mechanisms. Diabetic mice were induced by STZ injection. After treatment (5 or 25 mg/kg/day i.g) Saline containing 0.5 % carboxymethyl cellulose (CMC) for 2 months, hearts detected stress using western blot, Masson's trichrome staining Dihydroethidium (DHE) staining. vitro experiments, proliferation differentiation fibroblasts under different conditions through 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay immunofluorescence Administration significantly mitigated level, interstitial expressions related proteins STZ-induced hearts. exhibited anti-proliferative on primary mouse inhibiting reactive oxygen species (ROS)/extracellular regulated kinase (ERK) pathway ameliorated myofibroblast suppressing ROS/ERK/ transforming growth factor β (TGF-β)/periostin pathway. Increased ROS production, activation ERK/TGF-β/periostin myocardial are important events DCM. Alleviated genesis prevents regulating signaling Thus, ROS/periostin may represent novel approach reverse