Polybrominated diphenyl ethers are known to be toxic and impair thyroid function. However, the underlying molecular mechanisms are not well understood. We constructed a female Sprague-Dawley rat model to evaluate the role of endoplasmic reticulum stress, apoptosis and autophagy in 2,2′,4,4′-tetrabromodiphenylether (PBDE-47) induced thyroid toxicity. In the brain development spurt period (postnatal day 10), rats were treated with PBDE-47 (0, 1, 5, 10 mg/kg bw, i.g). Two addition groups were administered with 4-Phenylbutyric acid, an endoplasmic reticulum stress modulator, to reverse PBDE-47-induced thyroid toxicity. Our results demonstrated that PBDE-47 significantly decreased serum thyroid stimulating hormone levels, induced histologic changes in thyroid tissues, increased the percentage of cell apoptosis and expression levels of C/EBP-homologous protein, caspase 3, glucose-regulated protein 78, inositol-requiring enzyme 1, and autophagy-related proteins Beclin1 and 1A/1B-light chain 3. Besides of decreased serum thyroid stimulating hormone levels, all these changes were reversed by 4-Phenylbutyric acid. Taken together, these data indicate that, PBDE-47 damages the thyroid tissues by triggering endoplasmic reticulum stress, apoptosis and autophagy.

已知多溴联苯醚有毒并损害甲状腺功能。然而，潜在的分子机制还没有被很好地理解。我们构建了雌性Sprague-Dawley大鼠模型，以评估内质网应激，凋亡和自噬在2,2'，4,4'-四溴二苯醚（PBDE-47）诱导的甲状腺毒性中的作用。在大脑发育突增期（出生后第10天），用PBDE-47（0、1、5、10 mg / kg体重，ig）对大鼠进行治疗。另外两个组施用4-苯基丁酸（内质网应激调节剂），以逆转PBDE-47诱导的甲状腺毒性。我们的结果表明，PBDE-47显着降低了血清甲状腺刺激激素水平，诱导了甲状腺组织的组织学改变，增加了细胞凋亡百分比和C / EBP同源蛋白，半胱天冬酶3，葡萄糖调节蛋白78，需要肌醇的酶1和自噬相关蛋白Beclin1和1A / 1B轻链3的表达水平。血清甲状腺刺激激素水平，所有这些变化均被4-苯基丁酸逆转。综上所述，这些数据表明，PBDE-47通过触发内质网应激，凋亡和自噬而损害甲状腺组织。