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The effect of 131I-induced hypothyroidism on the levels of nitric oxide (NO), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), total nitric oxide synthase (NOS) activity, and expression of NOS isoforms in rats.
Biomolecules and Biomedicine ( IF 3.4 ) Pub Date : 2018-11-07 , DOI: 10.17305/bjbms.2018.2350
Jing Zhou 1 , Gang Cheng , Hua Pang , Qian Liu , Ying Liu
Affiliation  

Accumulating evidence has shown that hypothyroidism affects the cardiovascular system, significantly increasing the incidence of cardiovascular diseases. In the present study we investigated the effect of radioactive iodine (I-131)-induced hypothyroidism on several parameters of vascular function, such as nitric oxide (NO), total nitric oxide synthase (NOS) activity and expression of NOS isoforms, as well as on interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) as indicators of inflammation, in rats. A dose of 150 µCi of 131-I was determined as optimal for establishing the model of hypothyroidism in rats. After administration of 131-I, at the end of month 1, 2, and 4 (n = 3 for each time point), NO, IL-6, and TNF-α in the serum and total NOS activity in the aorta were determined in 150 µCi group, compared to controls. The mRNA and protein expression of endothelial, neuronal, and inducible NOS (eNOS, nNOS, and iNOS) in the rat aorta was also estimated, using quantitative reverse transcription polymerase chain reaction and Western blot, respectively. The levels of IL-6 and TNF-α increased in 150 µCi group; the results were significant at the end of month 2 and 4 for IL-6, and at all time points for TNF-α. The levels of NO decreased significantly at the end of month 2 and 4 in 150 µCi group. The total NOS activity increased significantly in 150 µCi group, at all three time points. Significant changes in the mRNA and protein expression of all three NOS isoforms were observed in 150 µCi group compared to controls. NO, IL-6, TNF-α levels and NOS activity and expression are altered in hypothyroid state, and the underlying mechanism should be further investigated.

中文翻译:

131I引起的甲状腺功能减退对一氧化氮(NO),白介素6(IL-6),肿瘤坏死因子α(TNF-α),总一氧化氮合酶(NOS)活性以及NOS亚型表达的影响大鼠。

越来越多的证据表明,甲状腺功能减退会影响心血管系统,从而大大增加心血管疾病的发病率。在本研究中,我们调查了放射性碘(I-131)引起的甲状腺功能减退对血管功能的几个参数的影响,例如一氧化氮(NO),总一氧化氮合酶(NOS)活性和NOS亚型的表达如白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)一样,在大鼠中作为炎症指标。确定建立150-Ci 131-I剂量是建立大鼠甲状腺功能减退模型的最佳方法。施用131-I后,在第1、2和4个月末(每个时间点n = 3)结束时,测定血清中的NO,IL-6和TNF-α以及主动脉中的总NOS活性在150 µCi组中,与对照组相比。还分别使用定量逆转录聚合酶链反应和蛋白质印迹法评估了大鼠主动脉中内皮,神经元和诱导型NOS(eNOS,nNOS和iNOS)的mRNA和蛋白表达。150 µCi组的IL-6和TNF-α含量升高;结果在IL-6的第2和4个月末以及TNF-α的所有时间点均显着。150 µCi组的2月和4月末NO含量显着下降。在所有三个时间点,150 µCi组的总NOS活性均显着增加。与对照组相比,在150 µCi组中观察到所有三种NOS亚型的mRNA和蛋白质表达均发生了显着变化。在甲状腺功能减退状态下,NO,IL-6,TNF-α水平以及NOS活性和表达发生改变,其潜在机制有待进一步研究。
更新日期:2020-08-21
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