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. 2020 May 25;11:345. doi: 10.3389/fphys.2020.00345

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Copyright © 2020 Kolijn, Kovács, Herwig, Lódi, Sieme, Alhaj, Sandner, Papp, Reusch, Haldenwang, Falcão-Pires, Linke, Jaquet, Van Linthout, Mügge, Tschöpe and Hamdani.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Myocardial inflammation and oxidative stress in heart tissue from the rat model. (A) Interleukin 6 (IL-6). (B) Intercellular adhesion molecule 1 (ICAM1). (C) Vascular cell adhesion molecule 1 (VCAM1). (D) Tumor necrosis factor alpha (TNFα). (E) 3-nitrotyrosine. (F) Hydrogen peroxide (H₂O₂). (G) Lipid peroxide (LPO). (H) Reduced glutathione (GSH). Data are shown as mean ± SEM; n = 7–8 left ventricular (LV) samples/group. *P < 0.05, **P < 0.001, ***P < 0.0001 control untreated versus Dahl salt-sensitive (DSS) untreated and ^†P < 0.05, ^†⁣†P < 0.001, ^{†⁣†⁣†}P < 0.0001 before versus after sGC activator treatment.