STX0119 Ameliorates Arthritis in SKG Mice via Inhibiting T Helper 17.
10.1007/s13770-016-9086-0
- Author:
Faisal HAYAT
1
;
Seung Hoon LEE
;
Eun Jung LEE
;
Seok Jung KIM
;
KyungAh JUNG
;
Soon Kyu LEE
;
Jeehee YOUN
;
Jun Ki MIN
;
Mi La CHO
;
Dong Yun SHIN
Author Information
1. College of Pharmacy, Gachon University, Incheon, Korea. dyshin@gachon.ac.kr
- Publication Type:Original Article
- Keywords:
Rheumatoid arthritis;
Signal transducer and activator of transcription 3 inhibitor;
T helper 17;
Treg;
Immune modualtion
- MeSH:
Animals;
Arthritis*;
Arthritis, Rheumatoid;
Autoimmune Diseases;
Cytokines;
In Vitro Techniques;
Inflammation;
Interleukin-10;
Interleukin-17;
Interleukin-6;
Interleukins;
Joints;
Mice*;
STAT3 Transcription Factor;
Up-Regulation;
Zymosan
- From:
Tissue Engineering and Regenerative Medicine
2016;13(1):91-99
- CountryRepublic of Korea
- Language:English
-
Abstract:
Rheumatoid arthritis (RA) is an autoimmune disease with chronic and excessive inflammation. Upregulation of interleukin (IL)-17 is involved in the pathogenesis of RA. STX0119 is a specific inhibitor of signal transducer and activator of transcription 3 (STAT3) as a potential target for the treatment of RA. STAT3 is a member of DNA-binding molecules that regulates the expression of proinflammatory cytokines involved in the pathogenesis of RA. The objective of this study was to determine whether STX0119 could inhibit STAT3 and IL-17. We demonstrated that STX0119 decreased T helper (Th) 17 differentiation and IL-17 expression in vitro. STX0119 also improved the severity of zymosan induced arthritis and reduced joint inflammation. STX0119 reduced the proliferation of Th17 and phosphorylated STAT3 expression while increasing Treg differentiation and phosphorylated STAT5 expression. Moreover, STX0119 decreased the expression of IL-6 and -17 but not IL-10. These findings suggest that STX0119 can be used to treat autoimmune RA through inhibiting the activation of STAT3.
