Xi Yang1, Liu-Xue Yang2, Ji Wu3,4, Man-Li Guo5, Yong Zhang6, Shao-Gang Ma6. 1. Geriatrics Department of Endocrinology and Metabolism, The First Affiliated Hospital of Guangxi Medical University. Guangxi Key Laboratory of Precision Medicine in Cardio-cerebrovascular Diseases Control and Prevention. Guangxi Clinical Research Center for Cardio-cerebrovascular Diseases, Guangxi, China. 2. Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Guilin Medical University, Guilin, China. 3. Department of Thyroid and Breast Surgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, China. 4. Department of Thyroid and Breast Surgery, Nanjing Drum Tower Hospital, Suqian, China. 5. Department of Endocrinology and Metabolism, Suqian People's Hospital, Nanjing Drum Tower Hospital, Suqian, China. 6. Department of Endocrinology and Metabolism, Suqian First Hospital, Suqian, China.
Abstract
BACKGROUND: To explore the role of lidocaine on subacute thyroiditis (SAT) and the molecular mechanism. METHODS: SAT models were constructed by infecting adenovirus to thyroid follicular epithelial cells. Cells were randomly divided into five groups: model group, low lidocaine, middle lidocaine, high lidocaine, and a control group. Thyroid secretion related factors TG and TPO, T3 and T4 were separately determined by reverse transcription-polymerase chain reaction (RT-PCR) and radioimmunoassay. Flow cytometry was used to determine thyroid follicular epithelial cell apoptosis situation. RT-PCR and Western blot analysis were used to determine the expression of inflammatory cytokines and pyroptosis related factors interleukin (IL)-1α, IL-6, THF-α, ELAVL1, NLR family pyrin domain containing 3 (NLRP3), caspase-1, and IL-1β. RESULTS: Lidocaine decreased the relative level of TG, TPO, T3, and T4 in adenovirus-infected thyroid follicular epithelial cells. All levels of concentrations, including low, middle, and high, of lidocaine, significantly decreased the apoptosis rate of adenovirus-infected cells. Lidocaine dramatically reduced the protein expression of IL-1α, IL-6, THF-α, ELAVL1, NLRP3, caspase-1, and IL-1β in adenovirus-infected thyroid follicular epithelial cells. CONCLUSION: Lidocaine can improve SAT through inhibiting expression of inflammatory factors and the pyroptosis pathway.
BACKGROUND: To explore the role of lidocaine on subacute thyroiditis (SAT) and the molecular mechanism. METHODS: SAT models were constructed by infecting adenovirus to thyroid follicular epithelial cells. Cells were randomly divided into five groups: model group, low lidocaine, middle lidocaine, high lidocaine, and a control group. Thyroid secretion related factors TG and TPO, T3 and T4 were separately determined by reverse transcription-polymerase chain reaction (RT-PCR) and radioimmunoassay. Flow cytometry was used to determine thyroid follicular epithelial cell apoptosis situation. RT-PCR and Western blot analysis were used to determine the expression of inflammatory cytokines and pyroptosis related factors interleukin (IL)-1α, IL-6, THF-α, ELAVL1, NLR family pyrin domain containing 3 (NLRP3), caspase-1, and IL-1β. RESULTS:Lidocaine decreased the relative level of TG, TPO, T3, and T4 in adenovirus-infected thyroid follicular epithelial cells. All levels of concentrations, including low, middle, and high, of lidocaine, significantly decreased the apoptosis rate of adenovirus-infected cells. Lidocaine dramatically reduced the protein expression of IL-1α, IL-6, THF-α, ELAVL1, NLRP3, caspase-1, and IL-1β in adenovirus-infected thyroid follicular epithelial cells. CONCLUSION:Lidocaine can improve SAT through inhibiting expression of inflammatory factors and the pyroptosis pathway.