TSP-2 suppresses the expression and DNA-binding activity of nuclear factor-κB p65 protein in mice with ulcerative colitis.
- Author:
Mingguang LAI
1
;
Lisheng WANG
;
Jun YAO
;
Chen WEI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Colitis, Ulcerative; immunology; metabolism; Male; Mice; Mice, Inbred BALB C; Rabbits; Thrombospondins; pharmacology; Transcription Factor RelA; genetics; metabolism
- From: Journal of Southern Medical University 2013;33(3):428-431
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of TSP-2, the antibody of Toll-like receptor 2 extracellular domain, on the expression and DNA-binding activity of nuclear factor-κB (NF-κB) p65 protein in mice with ulcerative colitis (UC).
METHODSSixty BALB/c mice were randomized equally into normal control group, UC model group, TSP-2 treatment group, and rabbit IgG treatment group. In the latter 3 groups, the mice were fed with 5% DSS (C6H7Na3O14S3) solution for 7 days to induced UC, followed then by treatment with daily injections of TSP-2 or rabbit IgG as appropriate for 7 days. The disease activity index was recorded during the treatment. The colitis tissues were collected after the treatments for HE staining and detecting the expression and DNA-binding activity of NF-κB p65 in the colon mucosa by Western blotting and ELISA.
RESULTSThe DNA binding activity and expressions of NF-κB P65 protein increased significantly in UC model group (P<0.05). TSP-2 treatment group significantly decreased the disease activity index (P<0.05) and lowered the DNA-binding activity and expression of NF-κB P65 protein (P<0.05) in the UC mouse models, while rabbit IgG produced no such effects (P>0.05).
CONCLUSIONTSP-2 can suppress the DNA-binding activity and protein expressions of NF-κB P65 and regulate excessive immune response in the intestines to ameliorate ulcerative colitis in mice.