| First Author | Wu R | Year | 2013 |
| Journal | Mol Immunol | Volume | 56 |
| Issue | 4 | Pages | 340-6 |
| PubMed ID | 23911388 | Mgi Jnum | J:202099 |
| Mgi Id | MGI:5517491 | Doi | 10.1016/j.molimm.2013.05.006 |
| Citation | Wu R, et al. (2013) Triptolide ameliorates ileocolonic anastomosis inflammation in IL-10 deficient mice by mechanism involving suppression of miR-155/SHIP-1 signaling pathway. Mol Immunol 56(4):340-6 |
| abstractText | The model of ileocaecal resection (ICR) in IL-10(-/-) mice provides us a new way to investigate the postsurgical inflammation of intestinal anastomosis. As an extracts isolated from Tripterygium wilfordii Hook F (TWHF), triptolide has been used to treat Crohn's disease for years. Several mechanisms have been interpreted in previous studies. MiR-155, which can be inhibited by triptolide, has a powerful ability in regulating immune cells. As a target of miR-155, SHIP-1 is a potent inhibitor of many inflammatory pathways. MiR-155/SHIP-1 pathway plays an important role in the inflammatory conditions. We hypothesized that triptolide would ameliorate the postsurgical intestine inflammation especially the anastomosis inflammation by inhibition of miR-155/SHIP-1 pathway. Histological examination, as well as examination of calprotectin and MPO, demonstrated triptolide significantly reduced the severity of postsurgical intestine inflammation. Our data also suggested triptolide could suppress miR-155/SHIP-1 signaling pathway and attenuated expression of inflammatory cytokines in IL-10(-/-) mice performed ICR. |
