Background: Graves' disease (GD) is an autoimmune disease that affects more women than men. In our previous study, a potent bioactive androgen, 5α-dihydrotestosterone (DHT) showed a protective effect against GD in female BALB/c mice. Evidence indicates that abnormal oxidative stress and immunosuppressive cytokines (TGF-β, IL-35) play critical roles in the pathogenesis and development of GD. The purpose of this research is to measure these cytokines and oxidative stress markers to explore potential protective mechanisms of DHT in a BALB/c mouse model of GD. Methods: GD was induced in female BALB/c mice by intramuscular injection of an adenovirus expressing the A-subunit of the TSH receptor (Ad-TSHR289). DHT or a matching placebo was injected every 3 days. Mice were sacrificed four weeks after the third virus immunization to obtain blood, thyroid and spleen for further analysis. Results: Thyroid hormones were significantly reduced in DHT treated GD mice. In addition, DHT attenuated thyroid oxidative injuries in GD mice, as shown by decreased total antioxidation capability (TAOC), superoxide dismutase (SOD) and the level of malondialdehyde (MDA). The levels of immunosuppressive cytokines (TGF-β, IL-35) in DHT group were significant higher compared with the GD group. Conclusions: The results demonstrated that DHT could reduce the severity of GD in female BALB/c mice by regulating oxidative stress. The upregulation of immunosuppressive cytokines might be another important protective mechanism.

中文翻译：

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二氢睾丸激素可调节Graves病雌性BALB / c小鼠模型中的氧化应激和免疫抑制细胞因子。

背景：格雷夫斯病（GD）是一种自身免疫性疾病，影响女性的人数多于男性。在我们之前的研究中，强效的生物活性雄激素5α-二氢睾丸激素（DHT）在雌性BALB / c小鼠中显示出对GD的保护作用。有证据表明，异常的氧化应激和免疫抑制细胞因子（TGF-β，IL-35）在GD的发病和发展中起关键作用。这项研究的目的是测量这些细胞因子和氧化应激标记物，以探讨GD的BALB / c小鼠模型中DHT的潜在保护机制。方法：通过肌内注射表达TSH受体A亚基的腺病毒（Ad-TSHR289）在雌性BALB / c小鼠中诱导GD。每3天注射DHT或匹配的安慰剂。第三次病毒免疫四周后处死小鼠以获取血液，甲状腺和脾脏作进一步分析。结果：在DHT治疗的GD小鼠中，甲状腺激素显着降低。此外，DHT可减轻GD小鼠的甲状腺氧化损伤，如总抗氧化能力（TAOC），超氧化物歧化酶（SOD）和丙二醛（MDA）含量降低所显示。与GD组相比，DHT组的免疫抑制细胞因子（TGF-β，IL-35）水平显着更高。结论：结果表明，DHT可以通过调节氧化应激降低BALB / c雌性小鼠中GD的严重程度。免疫抑制细胞因子的上调可能是另一个重要的保护机制。如总抗氧化能力（TAOC），超氧化物歧化酶（SOD）和丙二醛（MDA）含量降低所显示。与GD组相比，DHT组的免疫抑制细胞因子（TGF-β，IL-35）水平显着更高。结论：结果表明，DHT可以通过调节氧化应激降低BALB / c雌性小鼠中GD的严重程度。免疫抑制细胞因子的上调可能是另一个重要的保护机制。如总抗氧化能力（TAOC），超氧化物歧化酶（SOD）和丙二醛（MDA）含量降低所显示。与GD组相比，DHT组的免疫抑制细胞因子（TGF-β，IL-35）水平显着更高。结论：结果表明，DHT可以通过调节氧化应激降低BALB / c雌性小鼠中GD的严重程度。免疫抑制细胞因子的上调可能是另一个重要的保护机制。