Protective effects of toll like receptor 4 monoclonal antibodies on gut mucosal nuclear factor kappa B signaling pathway in mice with dextran sulfate sodium-induced acute ulcerative colitis
Lian Zhong
Abstract
Lian Zhong
Abstract
Objective To evaluate the effects of toll like receptor 4 monoclonal antibodies(TLR4mAb)on phosphorylated IκB kinase(p-IKK)and nuclear factor kappa B(NF-κB)in NF-κB signaling pathway in mice with dextran sulfate sodium(DSS)-induced acute ulcerative colitis(UC).Methods Thirty male BALB/c mice were randomly assigned to five groups:normal control group(A),model group(B),low dose(C),medium dose(D),and high dose(E)TLR4mAb groups.Mice in group B,C,C,and E were given 5.0%(wt/wt)DSS solution for 7 days to induce acute intestinal inflammation,and those in group A were given distilled water freely.Group C,D,E received TLR4mAb injection of corresponding doses.Daily disease activity index(DAI)and histopathological score(HPS)were observed.The protein expression of p-IKK was examined by Western blotting assay,and the activity of NF-κB was measured by EMSA.Results ① Compared with group A,group B had markedly higher DAI and HPS(P0.01).The HPS in group D and E was significantly lower than that of group B(P0.01).② The expression of protein p-IKK and the activity of NF-κB in group D and E were significantly lower than those in group B(P0.05 or 0.01).Conclusion TLR4mAb can ameliorate the DSS-induced colitis in mice through down-regulating the expression of p-IKK and the activity of NF-κB,reducing the downstream inflammatory factor expression.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To evaluate the effects of toll like receptor 4 monoclonal antibodies(TLR4mAb)on phosphorylated IκB kinase(p-IKK)and nuclear factor kappa B(NF-κB)in NF-κB signaling pathway in mice with dextran sulfate sodium(DSS)-induced acute ulcerative colitis(UC).Methods Thirty male BALB/c mice were randomly assigned to five groups:normal control group(A),model group(B),low dose(C),medium dose(D),and high dose(E)TLR4mAb groups.Mice in group B,C,C,and E were given 5.0%(wt/wt)DSS solution for 7 days to induce acute intestinal inflammation,and those in group A were given distilled water freely.Group C,D,E received TLR4mAb injection of corresponding doses.Daily disease activity index(DAI)and histopathological score(HPS)were observed.The protein expression of p-IKK was examined by Western blotting assay,and the activity of NF-κB was measured by EMSA.Results ① Compared with group A,group B had markedly higher DAI and HPS(P0.01).The HPS in group D and E was significantly lower than that of group B(P0.01).② The expression of protein p-IKK and the activity of NF-κB in group D and E were significantly lower than those in group B(P0.05 or 0.01).Conclusion TLR4mAb can ameliorate the DSS-induced colitis in mice through down-regulating the expression of p-IKK and the activity of NF-κB,reducing the downstream inflammatory factor expression.
Key concepts: IκB kinase, Ulcerative colitis, Medicine, Receptor, Colitis, Group B, NF-κB, IκBα