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NADPH Oxidase Inhibitor Apocynin Attenuates PCB153-Induced Thyroid Injury in Rats
Ablikim Abliz1, Chen Chen1, Wenhong Deng1
1Department of General Surgery, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, Hubei 430060, China.
Abstract:
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.
Insights
Polychlorinated biphenyls (PCBs) disrupt thyroid hormone homeostasis. Apocynin treatment inhibited NADPH oxidase (NOX) and NF-κB pathways, attenuating PCB-induced thyroid dysfunction in rats.
Area of Science:
- Environmental toxicology
- Endocrinology
- Molecular biology
Background:
- Polychlorinated biphenyls (PCBs) are persistent environmental pollutants known as endocrine disruptors.
- PCBs disrupt thyroid hormone (TH) homeostasis in humans and animals, but the precise mechanisms remain unclear.
- NADPH oxidase (NOX) and the NF-κB pathway are hypothesized to be involved in PCB-induced thyroid dysfunction.
Purpose of the Study:
- To investigate the role of NADPH oxidase (NOX) and the NF-κB pathway in PCB-induced thyroid dysfunction.
- To evaluate the therapeutic potential of apocynin, a NOX inhibitor, in mitigating PCB toxicity.
- To elucidate the molecular mechanisms underlying PCB-induced thyroid disruption.
Main Methods:
- Sixty Sprague-Dawley rats were divided into four groups: control, PCB153 treated, apocynin + PCB153 treated, and apocynin treated.
- Evaluated serum thyroid hormone levels and thyroid tissue morphology (light and transmission electron microscopy).
- Assessed expression of NOX2, 8-OHdG, and NF-κB via immunohistochemical staining; detected oxidative stress markers and inflammatory cytokines.
Main Results:
- Apocynin treatment significantly reduced serum thyroid hormone levels and thyroid pathological/ultrastructural injuries.
- Apocynin decreased oxidative stress markers (MDA) and inflammatory cytokines.
- Apocynin inhibited the expression of NOX2, 8-OHdG, and NF-κB in thyroid tissue.
Conclusions:
- NADPH oxidase (NOX) inhibition by apocynin attenuates PCB-induced thyroid dysfunction in rats.
- This protective effect is likely due to the prevention of reactive oxygen species (ROS) generation and inhibition of the NF-κB pathway.
- Targeting NOX and the NF-κB pathway offers potential therapeutic strategies for PCB-induced thyroid dysfunction.
