的生物可用性调节甲状腺细胞对酸过量的敏感性
Romina Oglio1, Carla Rodriguez1, Leonardo Salvarredi2
1Nuclear Biochemistry Division, Argentine National Atomic Energy Commission, Buenos Aires, Argentina.
Chemico-biological interactions
|November 28, 2023
概括
(Se) 的生物可用性通过调节抗氧化剂基因表达和信号通路来影响甲状腺细胞对酸过量的敏感性. 补充Se有助于通过激活Nrf2和影响PI3K/AKT信号传递来保护甲状腺细胞免受酸诱导的损伤.
科学领域:
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
- 营养科学 营养科学
背景情况:
- 酸对甲状腺激素的合成至关重要;失衡会导致甲状腺病理.
- (Se) 对于甲状腺健康至关重要,调节氧化还原稳态.
- 过多的酸盐会降低酸同载体 (NIS) 的调节,这种效应在补充Se时会逆转.
- NOX4衍生反应性氧物种 (ROS) 参与胺诱导的NIS抑制.
研究的目的:
- 调查Se生物可用性在调节甲状腺细胞对多余的反应中的作用.
- 探索Se通过哪些机制影响甲状腺细胞 (FRTL-5) 中酸诱导的变化.
主要方法:
- 使用差异化小鼠甲状腺细胞系 (FRTL-5).
- 采用了siRNA介导的Nox4.4的沉默.
- 评估了各种基因 (TGF-β1,GPX1,TXRND1,PTP1B,PTEN,NIS) 的mRNA表达.
- 测量了活性氧物种 (ROS) 水平,Nrf2转录活性和AKT酸化.
- 研究了2-α-Iodohexadecanal (2-IHD) 和其抑制剂 (SB431542) 的作用.
主要成果:
- 补充剂逆转了诱导的TGF-β1,AKT酸化和ROS水平的增加,同时恢复了GPX1和TXRND1的表达.
- 化物诱导的Nrf2活性和单酶反应仅在Se补充细胞中;Se抑制NF-κB酸化.
- 过多的化物降低了酸酶活性和PTEN/PTP1B的表达; Se恢复了PTEN的表达.
- 2-IHD通过涉及TGF-β1信号的ROS独立机制减少了NIS表达,Se.部分减轻了这种效应.
结论:
- 它的生物可用性通过Nrf2激活增强了抗氧化剂基因表达.
- Se通过氧化还原机制调节PI3K/AKT信号传递和NIS表达.
- 它通过影响关键细胞通路,对过量起到保护作用.
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