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Observing the effect of resveratrol on colitis-associated colorectal cancer based on TLR4/MyD88/NF-κB signaling pathway

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Author:
No author available
Journal Title:
Anti-Tumor Pharmacy
Issue:
3
DOI:
10.3969/j.issn.2095-1264.2024.03.06
Key Word:
Toll样受体4/髓样分化因子88/核转录因子κB信号通路;白藜芦醇;炎症相关性结直肠癌;小鼠;Toll-like receptor 4/myeloid differential factor 88/nuclear factor-κB signaling pathway;Resveratrol;Coli-tis-associated colorectal cancer

Abstract: Objective To explore the effect of resveratrol(Res)on colitis-associated colorectal cancer(CAC)based on Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B(TLR4/MyD88/NF-κB)signaling pathway.Methods Mice were divided into Control group,Vehicle group,low-concentration Res group(Res low)and high-concen-tration Res group(Res high).Azoxymethane/Dextran Sodium Sulfate(AOM/DSS)was used to construct mice CAC model.Mice in the groups were treated with Res and distilled water by gavage,respectively.The number of colorectal tumors and colorectal status of mice in each group were compared;ELISA was used to detect interleukin(IL)-1β,IL-6,IL-10 and tu-mor necrosis factor-α(TNF-α)levels in serum;Immunohistochemical staining was used to detect cyclooxygenase-2(COX-2),Ki-67,E-cadherin protein levels in colorectal tissue;qRT-PCR and Western blotting was used to detect TLR4,MyD88,NF-κB levels in colorectal tissue.Results Compared with the Control group,the number of colorectal tumors was increased,and colon tissue damage was severe in the Vehicle group.The serum levels of TNF-α,IL-1β and IL-6 were in-creased in the Vehicle group,so as the expression levels of COX-2,Ki-67,TLR4,MyD88 and NF-κB in colorectal tissue.The expression levels of IL-10 and E-cadherin in colorectal tissue were decreased in the Vehicle group(P<0.05).Com-pared with the Vehicle group,the above indicators in Res low group and the Res high group were all relieved,which was ob-viously Res dose-dependent(P<0.05).Conclusion Res could reduce colonic inflammatory response,inhibit malignant pro-liferation and metastasis of colorectal cancer,thereby alleviating intestinal damage in CAC mice by inhibiting TLR4/MyD88/NF-κB pathway.

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