Alleviation of Dextran Sodium Sulfate-induced Ulcerative Colitis in Mice by Adenanthin
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Abstract:
The effects of adenanthin (Ade) extracted from Isodon adenanthus on ulcerative colitis and the associated mechanisms were examined. An animal model of ulcerative colitis was constructed by administering dextran sulfate sodium. After Ade intervention, colonic damage was observed by hematoxylin-eosin staining, and changes in the levels of inflammatory factors were detected using enzyme-linked immunoassay. HT-29 cells were used to construct in vitro intestinal models. The effects of Ade on the Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-κB (TLR4/MyD88/NF-κB) signaling pathway and related apoptotic proteins were evaluated using western blotting. In vivo experiments showed that the expression levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in the high-dose Ade treatment group were reduced to 617.71, 670.55, and 442.17 pg/mg, respectively. In addition, Ade led to a significant (P<0.01) decrease in the expression of TLR4/MyD88/NF-κB signaling pathway proteins and B-cell lymphoma 2 (Bcl-2)-associated X proteins (Bcl2-associated X, Bax) (P<0.01) and a significant increase in Bcl-2 expression (P<0.01). The expression levels of TLR4, Myd88, p-NF-κB/NF-κB, and Bax in the high-dose Ade group were decreased by 40.30%, 55.86%, 48.23%, and 49.45%, respectively, and the expression level of Bcl2 was increased by 102.37% compared with that in the low-dose Ade group. In summary, Ade reduces the expression of inflammatory factors by inhibiting the TLR4/MyD88/NF-κB signaling pathway, thus improving dextran sulfate sodium-induced ulcerative colitis in mice.
