Tian Xun, Li Ning, Su Rui, Dai Chenyang, Zhang Ruiguo
Tianjin Institute of Hepatology, Tianjin Second People's Hospital, Tianjin, China.
Department of Nuclear Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Int J Endocrinol. 2020 Jun 30;2020:9210572. doi: 10.1155/2020/9210572. eCollection 2020.
Selenium, as an antioxidant, has been implicated in the development of autoimmune thyroiditis (AIT). Many studies showed selenium supplementation could decrease thyroid autoantibodies in patients with AIT. However, the underlying mechanisms have not been well determined. Therefore, we performed a clinical study to investigate the possible mechanism of beneficial effects of selenium treatment on AIT patients.
Forty euthyroid patients with AIT were randomized into two groups. Group I was treated with 200 g/day selenium supplementation, and group II received a placebo over a 3-month period. Thyroid stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb), antithyroglobulin antibody (TgAb), malondialdehyde (MDA), total antioxidant capacity (TAC), and superoxide dismutase (SOD) were measured before and 3 months after treatments. Additionally, twenty healthy volunteers also served as a control group for the evaluation of such parameters in basic condition.
Totally, 32 patients (group I, = 18; group II, = 14) completed the clinical study and were incorporated into the statistics. MDA level was higher and SOD activity and TAC were lower in patients compared to healthy individuals. After 3 months, TPOAb titer significantly decreased within group I ( < 0.001) but did not change within group II (=0.001). There were also no statistically significant changes in TSH and TgAb titers within the two groups (all > 0.05). Additionally, decreased MDA level (from 6.8 ± 1.3 nmol/ml to 4.9 ± 0.7 nmol/ml; < 0.001) and increased TAC (from 10.0 ± 1.9 mmol/l to 12.9 ± 3.1 mmol/l; =0.003) and SOD activity (from 72.3 ± 10.3 U/ml to 84.3 ± 13.2 U/ml; =0.007) were simultaneously observed after 3 months' selenium treatment. Moreover, there was a negative correlation between TAC and TgAb/TPOAb and a positive correlation between MDA and TgAb/TPOAb in AIT patients.
Our findings support the hypothesis that selenium treatment could decrease TPOAb titer via enforcing the defense against oxidative stress in euthyroid patients with AIT, which may be a potential underlying mechanism.
硒作为一种抗氧化剂,与自身免疫性甲状腺炎(AIT)的发生发展有关。许多研究表明,补充硒可降低AIT患者的甲状腺自身抗体。然而,其潜在机制尚未完全明确。因此,我们进行了一项临床研究,以探讨硒治疗对AIT患者产生有益作用的可能机制。
40例甲状腺功能正常的AIT患者被随机分为两组。第一组患者每天补充200μg硒,第二组在3个月期间接受安慰剂治疗。在治疗前和治疗3个月后测量促甲状腺激素(TSH)、甲状腺过氧化物酶抗体(TPOAb)、抗甲状腺球蛋白抗体(TgAb)、丙二醛(MDA)、总抗氧化能力(TAC)和超氧化物歧化酶(SOD)。此外,20名健康志愿者也作为对照组,用于评估这些参数的基础状态。
共有32例患者(第一组18例;第二组14例)完成了临床研究并纳入统计分析。与健康个体相比,患者的MDA水平较高,SOD活性和TAC较低。3个月后,第一组患者的TPOAb滴度显著降低(P<0.001),而第二组患者的TPOAb滴度无变化(P=0.001)。两组患者的TSH和TgAb滴度也无统计学显著变化(均P>0.05)。此外,经过3个月的硒治疗后,同时观察到MDA水平降低(从6.8±1.3nmol/ml降至4.9±0.7nmol/ml;P<0.001),TAC升高(从10.0±1.9mmol/l升至12.9±3.1mmol/l;P=0.003)以及SOD活性升高(从72.3±10.3U/ml升至84.3±13.2U/ml;P=0.007)。此外,在AIT患者中,TAC与TgAb/TPOAb之间呈负相关,MDA与TgAb/TPOAb之间呈正相关。
我们的研究结果支持以下假设:硒治疗可通过增强对甲状腺功能正常的AIT患者氧化应激的防御能力来降低TPOAb滴度,这可能是一种潜在的机制。