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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

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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.

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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.

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Available 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.

Key concepts: IκB kinase, Ulcerative colitis, Medicine, Receptor, Colitis, Group B, NF-κB, IκBα

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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 — Research Paper | ScholarLens