Abstract
Dihydroartemisinin (DHA) is the first generation of naturally occurring artemisinin derivatives with antimalarial activity. Recent research showed that this drug also features immunosuppressive and anti-inflammatory properties. Autoimmune thyroiditis (AIT) is a common organ-specific autoimmune disease with no available effective drug treatment. In this study, we investigated effects of DHA on AIT in vitro and in vivo. Results showed that DHA can visibly reduce antithyroglobulin antibody and thyroid peroxidase antibody levels and regulate T helper cells (Th) 1/Th2 imbalance of experimental AIT mice. DHA also dose-dependently suppressed proliferation of lymphocytes induced by lipopolysaccharide and concanavalin A. DHA inhibited binding of C-X-C chemokine ligand 10 (CXCL10) and its receptor (C–X–C motif) receptor 3 (CXCR3), thus inhibiting calcium flow. DHA can also reduce expression levels of PI3-kinase (PI3K), p-PI3K, protein kinase B (AKT), p-AKT, nuclear factor (NF)-κB/p65, and p-NF-κB/p65. In conclusion, DHA may serve as treatment drug for AIT by inhibiting the CXCR3/PI3K/AKT/NF-kB signaling pathway.
Highlights
Autoimmune thyroiditis (AIT) is a common organspecific autoimmune disease and a type of autoimmune thyroid disease (AITD)
experimental AIT (EAT) induced by thyroglobulin (Tg) immunization and NaI is a classical and widely used animal model in studies of AIT pathogenesis
Using the EAT mouse model, the current study investigated therapeutic effects of DHA on AITD and its potential mechanisms
Summary
Autoimmune thyroiditis (AIT) is a common organspecific autoimmune disease and a type of autoimmune thyroid disease (AITD). Clinical types of AITD include Hashimoto’s thyroiditis (HT), Grave’s disease, and atrophic thyroiditis; many factors, such as genetic and environmental factors, are suspected to play important roles in AITD [1]. HT, which is chronic lymphocytic thyroiditis, is the most common clinical type with high prevalence of 13.4%. Primary treatment methods for AITD include thyroid hormone replacement therapy (only for patients with hypothyroidism), immunosuppressive therapy, and glucocorticoid therapy. Novel and low-toxicity drugs should be developed for AITD treatment
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
