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. 2015 Dec 17;6(12):e2025. doi: 10.1038/cddis.2015.372

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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The protective effects of taurine on ischemic HCMs are TonEBP dependent. The knockdown of TonEBP decreased the ratio of cell viability (a, N=3), increased the LDH release level (b, N=3), increased the DNA fragmentation (c, N=3) and Annexin V-FITC and PI staining (d, N=3). Taurine supplementation could decrease the ratio of cell death and apoptosis (d, N=3). In the oxidative stress tests, TonEBP knockdown could exacerbate ROS production (e, N=3), calcium overload (f, N=3) and ATP depletion (g, N=3), associated with increased levels of caspase-3 (h, N=3). Similarly, both the Bax/Bcl-2 ratio (i and j, N=3) and cytochrome c release (i, k, N=6) were enhanced in TonEBP knockdown groups. With TonEBP knockdown, the further treatment of taurine no longer reverse the myocardial injury caused by OGD (b–h). (Data were expressed as mean±S.E.M. *P<0.05; **P<0.01; NS, no significance; OGD, oxygen glucose deprivation; Tau, taurine; Vec, vector)