Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO-1. (24th September 2017)

• Record Type: Journal Article
• Authors: Liao, Hai-han; Zhu, Jin-xiu; Feng, Hong; Ni, Jian; Zhang, Nan; Chen, Si; Liu, Huang-jun; Yang, Zheng; Deng, Wei; Tang, Qi-Zhu
• Other Names: Hrelia Silvana Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2017(2017)
• Publication Date: 2017-09-24
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2017/8370593
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Diabetic cardiomyopathy (DCM) is associated with a greater risk of mortality in patients with diabetes mellitus. Currently, no specific treatment has been suggested for DCM treatment. This study demonstrated that myricetin (M) attenuated DCM-associated cardiac injury in mice subjected to streptozotocin (SZT) and in neonatal rat cardiomyocytes (NRCM) challenged with high glucose. In vivo investigation demonstrated 6 months of M treatment (200 mg/kg/d) significantly alleviated cardiac hypertrophy, apoptosis, and interstitial fibrosis. Mechanically, M treatment significantly increased the activity of Nrf2/HO-1 pathway, strengthening antioxidative stress capacity evidenced by reversed activities of GPx and SOD, and decreased MDA production. M treatment also inhibited I κ B α /NF- κ B pathway, resulting in reduced secretion of inflammation cytokines including IL-1 β, TNF- α, and IL-6. Besides, the TGF β /Smad3 signaling was also blunted in DCM mice treated with M. These beneficial effects of M treatment protected cardiomyocytes from apoptosis as shown by decreased TUNEL-positive nucleus, c-caspase 3, and Bax. Similar effects of M treatment could be reproduced in NRCM treated with high glucose. Furthermore, through silencing Nrf2 in NRCM, we found that the regulation of I κ B α /NF κ B by M was independent on its function on Nrf2. Thus, we concluded that M possesses potential protective effects on DCM through inhibiting I κ B α /NF κ B and enhancing Nrf2/HO-1.