@article{ATM11486,
author = {Yang Xu and Hongxia Dong and Changhui Ge and Yan Gao and Haifeng Liu and Weiguang Li and Chenggang Zhang},
title = {CBLB502 administration protects gut mucosal tissue in ulcerative colitis by inhibiting inflammation},
journal = {Annals of Translational Medicine},
volume = {4},
number = {16},
year = {2016},
keywords = {},
abstract = {Background: Ulcerative colitis (UC) is a nonspecific inflammatory disease for which medications and therapeutic strategies have only been moderately successful. CBLB502, a toll-like receptor 5 (TLR5) agonist derived from Salmonella flagellin, exhibits anticancer and radioprotective activities via modulation of TLRs and the nuclear factor kappa B (NF-κB) signaling pathway and can protect against acute renal ischemic failure. In this study, we intend to examine the effects of CBLB502 on both TLR responses and the interleukin (IL) and NF-κB signaling pathways in UC treatment.
Methods: The UC mouse model was prepared in BALB/c mice by administering 2,4,6-trinitrobenzene sulfonic acid (TNBS). CBLB502 was used as the therapeutic drug. After CBLB502 therapy, the IL and tumor necrosis factor-α (TNF-α) levels were measured by ELISA. Total RNA and protein of colon samples was extracted.
Results: We found that CBLB502 had a distinctive therapeutic effect in the UC model. In control group animals, IL-10 expression in serum was 91.48±24.38 ng/mL; this was higher than in the model group (59.36±14.46 ng/mL, P},
issn = {2305-5847}, url = {https://atm.amegroups.org/article/view/11486}
}