Sauchinone ameliorates intestinal inflammation and promotes Th17 cell production of IL-10 via Blimp-1
| Autor: | Zhou Zhou, Jinxia Wang, Caiping Gao, Zhenzhen Guo, Yanxi Chen, Jie Xiao |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_treatment Cell Biophysics Dioxoles Biology Biochemistry Inflammatory bowel disease 03 medical and health sciences Mice 0302 clinical medicine PRDM1 medicine T helper 17 cell Animals Humans Benzopyrans Colitis Molecular Biology Inflammation Lamina propria Cell Biology medicine.disease Inflammatory Bowel Diseases Interleukin-10 Intestines Interleukin 10 030104 developmental biology Cytokine medicine.anatomical_structure Trinitrobenzenesulfonic Acid 030220 oncology & carcinogenesis Immunology Th17 Cells Positive Regulatory Domain I-Binding Factor 1 Signal Transduction |
| Zdroj: | Biochemical and biophysical research communications. 522(2) |
| ISSN: | 1090-2104 |
| Popis: | Inflammatory bowel disease (IBD) is characterized by chronic, unpredictable relapsing and inflammatory disease of the gastrointestinal tract. Daily diet patterns have long been one of the most important hotspots for IBD therapeutic strategies. Sauchinone (SAU), a key bioactive lignin isolated from the roots of the herb Saururus chinensis, has been known to play an anti-inflammatory role in several diseases. However, its effect on IBD has not yet been investigated. In the current study, we established 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice and treated them with SAU. Flow cytometric analysis was performed to determine the phenotype of T cells in the lamina propria. qRT-PCR and ELISA were performed to measure cytokine transcript and protein levels, respectively. We found that SAU ameliorated TNBS-induced mouse colitis and inflammatory responses in mucosal tissues and peripheral blood CD4+ T cells from IBD patients. SAU significantly suppressed Th17 differentiation but facilitated IL-10 production, and SAU-treated Th17 cells exhibited inhibitory functions in vitro and in vivo. Mechanistically, we demonstrated that SAU induced Blimp-1 expression (encoded by Prdm1) in Th17 cells, and SAU failed to increase IL-10 production in Prdm1-knockout Th17 cells. Our data reveal an uncharacterized mechanism through which SAU regulates intestinal inflammation and Th17 differentiation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect