The protective effect of naringenin on ulcerative colitis in mice through increasing Nrf2 pathway activity

Authors:
Open Access
Publisher website
Google Scholar
Abstract
Ulcerative colitis (UC) is a chronic inflammatory disease with an increasing prevalence worldwide. Naringenin (NAR) has been proven effective in preventing UC, but its mechanism has not been fully elucidated.Network pharmacology and bioinformatics methods were used to screen the genes associated with NAR and UC. A mouse model of dextran sulfate sodium (DSS)-induced ulcerative colitis was established. After treatment with NAR, the disease activity index (DAI) was scored, and colonic histopathology was observed via hematoxylin‒eosin (HE) staining. The expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and inflammation-related factors in the colons of UC mice was examined via western blotting and immunohistochemistry (IHC). The results of the animal experiments revealed that the model group of UC mice presented the most severe weight loss and the highest DAI scores. After the administration of NAR, weight loss was alleviated, and DAI scores were reduced (P < 0.05). NAR improved pathological manifestations in the mouse colon, such as reducing inflammatory cell infiltration and restoring goblet cell loss (P < 0.05). NAR significantly increased the protein expression levels of Nrf2, heme oxygenase 1 (HO-1), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) in the colon (P < 0.05) but decreased the protein expression levels of nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) (P < 0.05). NAR increases the protein expression of Nrf2, HO-1 and NQO1 in the colon of UC mice while inhibiting the expression of NF-κB, TNF-α, and IL-1β, thus reducing inflammation. This protective effect of NAR alleviates the inflammatory response in UC model mice.

This publication has 41 references indexed in Scilit: