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BioMed Research International
Volume 2015, Article ID 895976, 12 pages
http://dx.doi.org/10.1155/2015/895976
Research Article

Icariin Intervenes in Cardiac Inflammaging through Upregulation of SIRT6 Enzyme Activity and Inhibition of the NF-Kappa B Pathway

1Center of Disease Prevention and Treatment, Shanghai Guanghua Hospital of Integrative Traditional Chinese and Western Medicine, Shanghai 200052, China
2Department of Geriatrics, Shanghai Institute of Geriatrics, Huadong Hospital, Fudan University, Shanghai 200040, China
3Department of Perinatal Medicine, Pregnancy Research Centre and University of Melbourne Department of Obstetrics and Gynaecology, Royal Women’s Hospital, Parkville, VIC 3052, Australia
4Medical College, China Three Gorges University, Yichang 443002, China
5Key Laboratory of Cellular and Molecular Biology, Huashan Hospital, Fudan University, Shanghai 200040, China
6Department of Diseases Prevention and Healthcare, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China

Received 19 June 2014; Revised 23 July 2014; Accepted 7 August 2014

Academic Editor: Javier González-Gallego

Copyright © 2015 Yang Chen 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.

Abstract

The aim of the study was to investigate the effect of icariin (ICA) on cardiac aging through its effects on the SIRT6 enzyme and on the NF-κB pathway. Investigating the effect of ICA on the enzymatic activity of histone deacetylase SIRT6 revealed a concentration of 10−8 mol/L ICA had a maximum activating effect on histone deacetylase SIRT6 enzymatic activity. Western analysis showed that ICA upregulated SIRT6 protein expression and downregulated NF-κB (p65) protein expression in animal tissues and cell models. ICA upregulated the expression of SIRT6 and had an inhibitory effect on NF-κB inflammatory signaling pathways as shown by decreasing mRNA levels of the NF-κB downstream target genes TNF-α, ICAM-1, IL-2, and IL-6. Those effects were mediated directly or indirectly by SIRT6. We provided evidence that inflammaging may involve a novel link between the effects of ICA on SIRT6 (a regulator of aging) and NF-κB (a regulator of inflammation).