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口服邻苯二甲酸二丁酯通过氧化应激加剧雌性Wistar大鼠的慢性淋巴细胞性甲状腺炎。

Oral exposure to dibutyl phthalate exacerbates chronic lymphocytic thyroiditis through oxidative stress in female Wistar rats.

作者信息

Wu Yang, Li Jinquan, Yan Biao, Zhu Yuqing, Liu Xudong, Chen Mingqing, Li Dai, Lee Ching-Chang, Yang Xu, Ma Ping

机构信息

Laboratory of Environment- immunological and neurological Diseases, School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, China.

Laboratory of Environmental Biomedicine, College of Life Sciences, Central China Normal University, Wuhan, 430079, China.

出版信息

Sci Rep. 2017 Nov 13;7(1):15469. doi: 10.1038/s41598-017-15533-z.

DOI:10.1038/s41598-017-15533-z
PMID:29133889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5684247/
Abstract

Chronic lymphocytic thyroiditis (CLT) is a common autoimmune disorder. The possible pathogenic role and mechanism of dibutyl phthalate (DBP) in CLT is still controversial. Experiments were conducted after 35-days of oral exposure to the three concentrations of DBP or saline, and three immunizations with thyroglobulin (TG). Healthy female Wistar rats were randomly divided into ten exposure groups (n = 8 each): (A) saline control, (B) 0.5 mg/kg/d DBP, (C) 5 mg/kg/d DBP, (D) 50 mg/kg/d DBP, (E) TG-immunized group, (F) TG- combined with 0.5 mg/kg/d DBP, (G) TG- combined with 5 mg/kg/d DBP, (H) TG- combined with 50 mg/kg/d DBP, (I) TG- combined with 50 mg/kg/d DBP plus 100 mg/kg/d vitamin C; (J) 100 mg/kg/d vitamin C. We showed that oral exposure DBP can aggravate CLT in rats. This deterioration was concomitant with increased thyroid auto antibodies, Th1/Th2 imbalance and Th17 immune response, activated pro-inflammatory and apoptosis pathways, and increased thyroid dysfunction in rats. Our results also suggested that DBP could promote oxidative damage. The study also found that vitamin C reduced the levels of oxidative stress and alleviated CLT. In short, the study showed that DBP exacerbated CLT through oxidative stress.

摘要

慢性淋巴细胞性甲状腺炎(CLT)是一种常见的自身免疫性疾病。邻苯二甲酸二丁酯(DBP)在CLT中可能的致病作用和机制仍存在争议。在口服三种浓度的DBP或生理盐水35天后,以及用甲状腺球蛋白(TG)进行三次免疫接种后进行实验。将健康雌性Wistar大鼠随机分为十个暴露组(每组n = 8):(A)生理盐水对照组,(B)0.5 mg/kg/d DBP组,(C)5 mg/kg/d DBP组,(D)50 mg/kg/d DBP组,(E)TG免疫组,(F)TG联合0.5 mg/kg/d DBP组,(G)TG联合5 mg/kg/d DBP组,(H)TG联合50 mg/kg/d DBP组,(I)TG联合50 mg/kg/d DBP加100 mg/kg/d维生素C组;(J)100 mg/kg/d维生素C组。我们发现口服DBP可加重大鼠的CLT。这种恶化伴随着大鼠甲状腺自身抗体增加、Th1/Th2失衡和Th17免疫反应、促炎和凋亡途径激活以及甲状腺功能障碍增加。我们的结果还表明DBP可促进氧化损伤。该研究还发现维生素C可降低氧化应激水平并减轻CLT。简而言之,该研究表明DBP通过氧化应激加剧了CLT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/e340525e3d84/41598_2017_15533_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/0aaba05a3118/41598_2017_15533_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/1d20780ee0fb/41598_2017_15533_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/096fc9051c12/41598_2017_15533_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/e6fed1cc2d6e/41598_2017_15533_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/f50d4463b51e/41598_2017_15533_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/e340525e3d84/41598_2017_15533_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/0aaba05a3118/41598_2017_15533_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/1d20780ee0fb/41598_2017_15533_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/096fc9051c12/41598_2017_15533_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/e6fed1cc2d6e/41598_2017_15533_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/f50d4463b51e/41598_2017_15533_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9c2/5684247/e340525e3d84/41598_2017_15533_Fig6_HTML.jpg

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