NADPH Oxidase Inhibitor Apocynin Attenuates PCB153-Induced Thyroid Injury in RatsReport as inadecuate

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International Journal of Endocrinology - Volume 2016 2016, Article ID 8354745, 11 pages -

Research ArticleDepartment of General Surgery, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, Hubei 430060, China

Received 28 October 2015; Accepted 11 February 2016

Academic Editor: Paul M. Yen

Copyright © 2016 Ablikim Abliz 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.


PCBs, widespread endocrine disruptors, cause the disturbance of thyroid hormone TH homeostasis in humans and animals. However, the exact mechanism of thyroid dysfunction caused by PCBs is still unknown. In order to clarify the hypotheses that NADPH oxidase NOX and subsequent NF-κB pathway may play roles in thyroid dysfunction, sixty Sprague-Dawley rats were randomly divided into four groups: control group, PCB153 treated PCB group, received apocynin with PCB153 treatment APO + PCB group, and drug control APO group. Serum thyroid hormone levels were evaluated. The morphological change of thyroid tissue was analyzed under the light and transmission electron microscopy. NOX2, 8-OHdG, and NF-κB expression in the thyroid tissue was evaluated by immune-histochemical staining. Oxidative stress and inflammatory cytokines were detected. The following results were reduced after apocynin treatment: 1 serum thyroid hormone, 2 thyroid pathological injuries, 3 thyroid MDA, 4 thyroid ultrastructural change, 5 serum inflammatory cytokines, and 6 thyroid expression of NOX2, 8-OHdG, and NF-κB. These results suggested that NOX inhibition attenuates thyroid dysfunction induced by PCB in rats, presumably because of its role in preventing ROS generation and inhibiting the activation of NF-κB pathway. Our findings may provide new therapeutic targets for PCBs induced thyroid dysfunction.

Author: Ablikim Abliz, Chen Chen, Wenhong Deng, Weixing Wang, and Rongze Sun



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