Dihydroartemisinin attenuates autoimmune thyroiditis by inhibiting the CXCR3/PI3K/AKT/NF-κB signaling pathway
Autor: | Yanrong Liu, Zhan-Hong Cui, Cheng Yang, Jing Meng, Shuang Chen, Jia-Huan Yang, Denghui Zhai, Qin Tian, Ai Xiaoyu, Tao Sun, Yuan Qin, Honggang Zhou, Huijuan Liu, Meng Li |
---|---|
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.medical_treatment Dihydroartemisinin Pharmacology CXCR3 PI3K NF-κB Autoimmune thyroiditis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine CXCL10 Protein kinase B PI3K/AKT/mTOR pathway Chemistry AIT food and beverages medicine.disease DHA 030104 developmental biology Oncology 030220 oncology & carcinogenesis Signal transduction Research Paper |
Zdroj: | Oncotarget |
ISSN: | 1949-2553 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |