Triptolide ameliorates ileocolonic anastomosis inflammation in IL-10 deficient mice by mechanism involving suppression of miR-155/SHIP-1 signaling pathway

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• 作者：Rong Wu ; Yi Li ; Zhen Guo ; Jianfeng Gong ; Weiming Zhu ; Ning Li ; Jieshou Li
• 关键词：Triptolide ; ICR in IL-10 deficient mice ; Crohn's disease ; MiR-155/SHIP-1 pathway
• 刊名：Molecular Immunology
• 出版年：2013
• 出版时间：31 December, 2013
• 年：2013
• 卷：56
• 期：4
• 页码：340-346
• 全文大小：1594 K

文摘

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.