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Wen Jing,Deng Chaonan,Shi Lixin,Zhou Shi,Zhang Miao,Hu Xiaoli,Wang Nianxue,Luo Lijuan 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.2
Background Hashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is one of the most common autoimmune disease (AITD) in clinical practice. It is urgent to explore the mechanism of amiodarone-induced thyroid dysfunction. Objective This study aims to assess the expression levels of miR-214 and FasL in amiodarone contact type of HT, and the effect of miR-214 on cell viability and apoptosis and potential mechanism. Results We found that miR-214 was low expressed in the tissues of amiodarone-treated thyroiditis patients. MiR-214 increased the survival rate of amiodarone-induced thyroid epithelial follicular cells and inhibited apoptosis. Mechanically, we found that miR-214 could bind to FASL and regulate MAPK signaling pathway through FASL. Conclusions Our results suggested that miR-214 could be a potential therapeutic target for Hashimoto's thyroiditis.