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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 2391820, 9 pages
https://doi.org/10.1155/2017/2391820
Research Article

The Preconditioning of Berberine Suppresses Hydrogen Peroxide-Induced Premature Senescence via Regulation of Sirtuin 1

1Department of Clinical Immunology, Research Center for Immunology, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China
2Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China
3Xinxiang Assegai Medical Laboratory Institute, Xinxiang Medical University, Xinxiang 453003, China
4Department of Microbiology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China

Correspondence should be addressed to Xiaofei Zhu; nc.ude.umxx@fxuhz

Received 20 April 2017; Accepted 23 May 2017; Published 2 July 2017

Academic Editor: Isabel C. F. R. Ferreira

Copyright © 2017 Xiaofei Zhu 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

With a long history of application in Chinese traditional medicine, berberine (BBR) was reported to exhibit healthspan-extending properties in some age-related diseases, such as type 2 diabetes and atherosclerosis. However, the antiaging mechanism of BBR is not completely clear. By means of hydrogen peroxide- (H2O2-) induced premature cellular senescence model, we found that a low-concentration preconditioning of BBR could resist premature senescence in human diploid fibroblasts (HDFs) measured by senescence-associated β-galactosidase (SA-β-gal), accompanied by a decrease in loss of mitochondrial membrane potential and production of intracellular reactive oxygen species (ROS). Moreover, the low-concentration preconditioning of BBR could make cells less susceptible to subsequent H2O2-induced cell cycle arrest and growth inhibition. Experimental results further showed that the low concentration of BBR could induce a slight increase of ROS and upregulate the expression level of sirtuin 1 (SIRT1), an important longevity regulator. H2O2-induced activation of checkpoint kinase 2 (Chk2) was significantly attenuated after the preconditioning of BBR. The present findings implied that the low-concentration preconditioning of BBR could have a mitohormetic effect against cellular senescence triggered by oxidative stress in some age-related diseases through the regulation of SIRT1.