title: Triptolide ameliorates ileocolonic anastomosis inflammation in IL-10 deficient mice by mechanism involving suppression of miR-155/SHIP-1 signaling pathway.
abstract: 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.
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, PR China.
authors.forename: Rong
authors.initials: R
authors.lastname: Wu
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
authors.forename: Zhen
authors.initials: Z
authors.lastname: Guo
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Gong
authors.forename: Weiming
authors.initials: W
authors.lastname: Zhu
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000714:Anastomosis, Surgical / Q000009:adverse effects / Q000379:methods; D000818:Animals; D015153:Blotting, Western; D003106:Colon / Q000601:surgery; D003424:Crohn Disease / Q000209:etiology / Q000235:genetics / Q000517:prevention & control*; D016207:Cytokines / Q000378:metabolism; D004224:Diterpenes / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D004852:Epoxy Compounds / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D007082:Ileum / Q000601:surgery; D000072181:Inositol Polyphosphate 5-Phosphatases; D016753:Interleukin-10 / Q000172:deficiency / Q000235:genetics; D039841:Leukocyte L1 Antigen Complex / Q000378:metabolism; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D018345:Mice, Knockout; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010616:Phenanthrenes / Q000494:pharmacology*; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases; D010744:Phosphoric Monoester Hydrolases / Q000235:genetics* / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology; D011183:Postoperative Complications / Q000209:etiology / Q000235:genetics / Q000517:prevention & control; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics; D029757:Tripterygium / Q000737:chemistry
chemical_list: D016207:Cytokines; D004224:Diterpenes; D004852:Epoxy Compounds; D039841:Leukocyte L1 Antigen Complex; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D010616:Phenanthrenes; D010936:Plant Extracts; D016753:Interleukin-10; C001899:triptolide; D009195:Peroxidase; D010744:Phosphoric Monoester Hydrolases; D000072181:Inositol Polyphosphate 5-Phosphatases; C000606433:Inpp5d protein, mouse; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
keywords: Crohn's disease; ICR in IL-10 deficient mice; MiR-155/SHIP-1 pathway; Triptolide