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Treatment of lidocaine on subacute thyroiditis via restraining inflammatory factor expression and inhibiting pyroptosis pathway
Author(s) -
Yang Xi,
Yang LiuXue,
Wu Ji,
Guo ManLi,
Zhang Yong,
Ma ShaoGang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27675
Subject(s) - pyroptosis , subacute thyroiditis , medicine , lidocaine , immunology , thyroiditis , inflammation , pharmacology , inflammasome , anesthesia , thyroid
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.