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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 8370593, 14 pages
Research Article

Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO-1

Hai-han Liao,1,2,3 Jin-xiu Zhu,1,2,3 Hong Feng,4 Jian Ni,1,2,3 Nan Zhang,1,2,3 Si Chen,2,3 Huang-jun Liu,1,2,3 Zheng Yang,1,2,3 Wei Deng,1,2,3 and Qi-Zhu Tang1,2,3

1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China
2Cardiovascular Research Institute of Wuhan University, Wuhan, China
3Hubei Key Laboratory of Cardiology, Wuhan, China
4Department of Gerontology, Renmin Hospital of Wuhan University, Wuhan 430060, China

Correspondence should be addressed to Qi-Zhu Tang; nc.ude.uhw@gnatzq

Received 12 May 2017; Revised 18 July 2017; Accepted 26 July 2017; Published 24 September 2017

Academic Editor: Silvana Hrelia

Copyright © 2017 Hai-han Liao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 IκBα/NF-κB pathway, resulting in reduced secretion of inflammation cytokines including IL-1β, TNF-α, and IL-6. Besides, the TGFβ/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 IκBα/NFκB by M was independent on its function on Nrf2. Thus, we concluded that M possesses potential protective effects on DCM through inhibiting IκBα/NFκB and enhancing Nrf2/HO-1.