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. 2017 Jun 22;66(4):303–312. doi: 10.1538/expanim.16-0102

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©2017 Japanese Association for Laboratory Animal Science

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/)

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Fig. 3. — Administration of EsA suppressed inflammation and oxidative stress in the kidney of rats with CLP-induced sepsis. (A) The levels of MDA and GSH and activities of MPO and SOD. (B) The contents of serum TNF-α, IL-1β, and IL-6. (C) The levels of kidney tissue TNF-α, IL-1β, and IL-6. (D) Immunohistochemical analysis of COX-2 and iNOS in the kidney. Scale bars: 50 µm. (E) The expression levels of COX-2 and iNOS in the kidney were assessed using western blotting. i, Sham group; ii, CLP-induced AKI group; iii, CLP-induced AKI + DXM (2 mg/kg) group; iv, CLP-induced AKI + EsA (2.5 mg/kg) group; v, CLP-induced AKI + EsA (5 mg/kg) group; vi, CLP-induced AKI + EsA (10 mg/kg) group. Data are shown as the mean ± SD. *P<0.05; **P<0.01; ***P<0.001.