The effect and mechanism of excessive iodine on the endothelial function of human umbilical vein endothelial cells

被引:3
|
作者
Wang, Dandan [1 ,2 ,3 ]
Li, Peng [4 ]
Liu, Lixiang [1 ,2 ,3 ]
Liu, Peng [1 ,2 ,3 ]
Zhou, Zheng [1 ,2 ,3 ]
Jin, Meihui [1 ,2 ,3 ]
Li, Baoxiang [1 ,2 ,3 ]
Li, Fan [1 ,2 ,3 ]
Chen, Yao [1 ,2 ,3 ]
Shen, Hongmei [1 ,2 ,3 ]
机构
[1] Harbin Med Univ, Ctr Endem Dis Control, Chinese Ctr Dis Control & Prevent, 157 Baojian Rd, Harbin 150081, Peoples R China
[2] Harbin Med Univ, Key Lab Etiol & Epidemiol, Natl Hlth Commiss & Educ Bur Heilongjiang Prov, Harbin, Peoples R China
[3] Harbin Med Univ, Heilongjiang Prov Key Lab Trace Elements & Human, Harbin, Peoples R China
[4] Xuzhou Med Univ, Sch Publ Hlth, Key Lab Environm & Hlth, Xuzhou, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
cardiovascular; endothelia function; inflammation; iodine excess; thyroid; SUBCLINICAL HYPOTHYROIDISM; RISK; DISEASE;
D O I
10.1002/tox.23671
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Iodine excess (IE) can cause thyroid dysfunction, thyroid diseases can adversely affect cardiovascular function. Accordingly, this study was to explore the direct and indirect effects of IE on endothelial function. Nthy-ori 3-1 and HUVECs cells were treated with potassium iodide (KI). CCK-8, LDH leakage, Elisa, RT-PCR and Western blotting were used to detect relevant indicators. Results showed that a certain level of KI can directly and indirectly reduce the viability of HUVECs and increase cytotoxicity. KI decreased the expression of ET-1 and VWF in HUVECs, inhibited the secretion of ET-1 in culture medium, and increased the expression of IL-6 and TNF alpha in HUVECs or Nthy-ori 3-1 cells alone. In the co-culture system, KI decreased the expression of ET-1 and THBD and increased the expression of TNF alpha and IL-6. Collectively, IE can directly and indirectly inhibit endothelial function of endothelial cells, which may be related to its induced inflammatory response.
引用
收藏
页码:136 / 145
页数:10
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