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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 7031397, 17 pages
http://dx.doi.org/10.1155/2016/7031397
Research Article

The Natural Polyphenol Epigallocatechin Gallate Protects Intervertebral Disc Cells from Oxidative Stress

1Department of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland
2Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Hikarigaoka, Fukushima City, Fukushima 960-1295, Japan
3Prodorso, Walchestrasse 15, 8006 Zurich, Switzerland
4Department of Rheumatology, University Hospital, Zurich, Switzerland

Received 20 November 2015; Revised 30 January 2016; Accepted 16 February 2016

Academic Editor: Nageswara Madamanchi

Copyright © 2016 Olga Krupkova 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

Oxidative stress-related phenotypic changes and a decline in the number of viable cells are crucial contributors to intervertebral disc degeneration. The polyphenol epigallocatechin 3-gallate (EGCG) can interfere with painful disc degeneration by reducing inflammation, catabolism, and pain. In this study, we hypothesized that EGCG furthermore protects against senescence and/or cell death, induced by oxidative stress. Sublethal and lethal oxidative stress were induced in primary human intervertebral disc cells with H2O2 (total ). Under sublethal conditions, the effects of EGCG on p53-p21 activation, proliferative capacity, and accumulation of senescence-associated β-galactosidase were tested. Further, the effects of EGCG on mitochondria depolarization and cell viability were analyzed in lethal oxidative stress. The inhibitor LY249002 was applied to investigate the PI3K/Akt pathway. EGCG inhibited accumulation of senescence-associated β-galactosidase but did not affect the loss of proliferative capacity, suggesting that EGCG did not fully neutralize exogenous radicals. Furthermore, EGCG increased the survival of IVD cells in lethal oxidative stress via activation of prosurvival PI3K/Akt and protection of mitochondria. We demonstrated that EGCG not only inhibits inflammation but also can enhance the survival of disc cells in oxidative stress, which makes it a suitable candidate for the development of novel therapies targeting disc degeneration.