Research Paper Volume 11, Issue 9 pp 2822—2835
Phloretin protects against cardiac damage and remodeling via restoring SIRT1 and anti-inflammatory effects in the streptozotocin-induced diabetic mouse model
- 1 Department of Pharmacy, Tongde Hospital of Zhejiang Province, Hangzho, Zhejiang 310012, China
- 2 Department of Rehabilitation, Tongde Hospital of Zhejiang Province, Hangzho, Zhejiang 310012, China
- 3 Department of Vascular Surgery, Tongde Hospital of Zhejiang Province, Hangzho, Zhejiang 310012, China
received: December 31, 2018 ; accepted: May 3, 2019 ; published: May 10, 2019 ;https://doi.org/10.18632/aging.101954
How to Cite
Copyright: Ying et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Diabetic cardiomyopathy increases the risk of heart failure independent of coronary artery disease and hypertension. Phloretin (PHL) shows anti-inflammatory effects in macrophages. In this study, we explored the protective effects of PHL on high glucose (HG)-induced injury in diabetic cardiomyopathy in vivo and in vitro. Using streptozotocin-induced diabetic mouse model and incubating cardiac cells line under a HG environment, PHL were evaluated of the activities of anti-inflammation and anti-fibrosis. In the study, PHL treatment ameliorated cardiomyocyte inflammation injury, and reduced fibrosis in vivo and in vitro. PHL also improved cardiac biochemical criterions after 8 weeks of induction of diabetes in C57BL/6 mice. Molecular docking results indicated that silent information regulator 2 homolog 1 (SIRT1) bound to PHL directly and that SIRT1 expression was upregulated in the PHL-treated group in HG-induced H9C2 cells. Protective effect of PHL was been eliminated in silence SIRT1 H9C2 cells. Taken together, these results suggested that PHL suppressed HG-induced cardiomyocyte injury via restoring SIRT1 expression.