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. 2016 Feb 17;16:63. doi: 10.1186/s12906-016-1032-1

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© Roh et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 7 — Predicted mechanism in pancreatic tissue on administering AH. Our study revealed that AHR suppresses STZ-induced type 1 diabetes. An important mechanism of AHR’s anti-diabetic effect is its capacity to reduce the oxidative stress state by diminishing ROS generation and lipid peroxidation in the pancreas. Our data further suggest that another critical mechanism of AHR’s anti-diabetic property is its ability to ameliorate inflammation through modulation of the serum TNF-α and IL-6 levels and the pancreatic protein expressions of NF-кB