Dihydroartemisinin attenuates autoimmune thyroiditis by inhibiting the CXCR3/PI3K/AKT/NF-κB signaling pathway
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Huijuan Liu1,2,*, Qin Tian1,*, Xiaoyu Ai1,*, Yuan Qin1, Zhanhong Cui1, Meng Li1, Jiahuan Yang1, Denghui Zhai1, Yanrong Liu3, Shuang Chen3, Jing Meng1, Tao Sun1,3, Honggang Zhou1,3 and Cheng Yang1,3
1State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, College of Life Sciences, Nankai University, Tianjin, China
2College of Life Sciences, Nankai University, Tianjin, China
3Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China
*These authors have contributed equally to this work
Cheng Yang, email: email@example.com
Honggang Zhou, email: firstname.lastname@example.org
Tao Sun, email: email@example.com
Keywords: DHA; AIT; CXCR3; PI3K; NF-κB
Received: September 19, 2017 Accepted: November 13, 2017 Published: December 01, 2017
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.
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