کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2538937 | 1122159 | 2011 | 7 صفحه PDF | دانلود رایگان |

Growing evidence suggests that TLRs/NF-κB signaling pathway plays a critical role in the pathogenesis of Crohn's disease (CD). We have reported that triptolide, an active component from Tripterygium wilfordii Hook, showed therapeutic activity in IL-10-deficeint (IL-10−/−) mice, a murine CD model. However the full mechanisms of action of this agent in CD remain largely unknown. We hypothesized that triptolide would ameliorate the experimental colitis by inhibiting TLRs/NF-κB signaling pathway. We found TLR2 and TLR4 were upregulated in IL-10−/− mice, triptolide inhibited the TLRs/NF-κB signaling pathway in vivo. In addition, triptolide in vitro was able to downregulate the TLRs/NF-κB pathway in cultured colonic explants from CD patients. Our results confirm the therapeutic effect of triptolide in experimental colitis, and suggest it as a promising compound for CD treatment. These findings also support the possibility that targeted inhibition of TLR signaling pathway is an approach deserving further investigation as a therapeutic strategy for CD.
Graphical AbstractTriptolide reduces the expression of TLR2 and TLR4 in the colon of IL-10−/− mice and cultured colonic explants from patients of Crohn's disease.Figure optionsDownload as PowerPoint slide
Journal: Fitoterapia - Volume 82, Issue 4, June 2011, Pages 709–715