Premium
The JAK2 inhibitor AG490 regulates the Treg/Th17 balance and alleviates DSS‐induced intestinal damage in IBD rats
Author(s) -
Guo Jing,
Wang Liyun,
Wu Jie,
Xu Lingfen,
Sun Mei
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13311
Subject(s) - medicine , inflammatory bowel disease , immunology , pathogenesis , rar related orphan receptor gamma , spleen , flow cytometry , rheumatoid arthritis , foxp3 , disease , immune system
The pathogenesis of inflammatory bowel disease (IBD) remains unclear, and it is currently believed that an imbalance in regulatory T (Treg) cells/T helper 17 cells (Th17 cells) is related to the occurrence and development of IBD. Recently, the JAK2 inhibitor AG490 has been used in animal models such as rheumatoid arthritis and bronchial asthma models and shown to exert immunoregulatory functions that improve disorder in the Treg/Th17 cell balance. This study aimed to evaluate the effect of AG490 on the intestinal inflammatory process in an IBD rat model. A dextran sulfate sodium (DSS)‐induced IBD rat model was established, and disease activity index (DAI) scores were calculated. The histopathological damage score was determined by haematoxylin‐eosin (H&E) staining. Treg/Th17 cells in the spleen were detected by flow cytometry. The levels of interleukin (IL)‐10, IL‐6 and IL‐17A were detected by enzyme‐linked immunosorbent assay (ELISA). AG490 attenuated DSS‐induced IBD injury by regulating the Treg/Th17 balance and related cytokine secretion to reduce the DAI and colonic tissue damage. Thus, AG490 may be a new method for effective treatment of IBD.