Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

Abstract EN

Background.

The nuclear factor kappa beta (NF-κB) signaling pathway plays an important role in ulcerative colitis (UC).

Huangkui Lianchang decoction (HLD) is an effective traditional Chinese medicinal compound used in the treatment of UC.

HLD has good effects in the clinic, but the mechanism by which HLD acts is unclear.

This study aims to reveal the exact molecular mechanism of HLD in the treatment of UC.

Methods.

Mouse ulcerative colitis was induced by dextran sulfate sodium (DSS) and treated with HLD.

Intestinal damage was assessed by disease activity index (DAI), colon macroscopic lesion scores, and histological scores.

Interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β were detected in colon tissue using ELISA.

Myeloperoxidase (MPO) and superoxide dismutase (SOD) activities in the colonic mucosa were measured.

The levels of IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in the colon were determined by real-time quantitative polymerase chain reaction (qPCR).

The expression of NF-κB, IκBα, and p-IκBα in the colon was measured by Western blot.

Results.

After treatment with HLD, the DAI scores, macroscopic lesion scores, and histological scores decreased, and the levels of inflammatory cytokines related to the NF-κB signaling pathway, such as IL-6, TNF-α, and IL-1β, as well as those of iNOS and COX-2, were reduced; at the same time, colonic pathological damage was alleviated, and the MPO and SOD activities decreased.

Western blot confirmed that HLD can inhibit the NF-κB signaling pathway in DSS-induced ulcerative colitis.

Conclusion.

HLD can alleviate the inflammation caused by ulcerative colitis.

In particular, high doses of HLD can significantly alleviate intestinal inflammation and have comparable efficacy to Mesalazine.

We propose that the anti-inflammatory activity of HLD on DSS-induced colitis in mice may involve the inhibition of the NF-κB pathway.