Efficacy of herb-partitioned moxibustion at Qihai (CV 6) and bilateral Tianshu (ST 25) on colonic damage and the TLR4/NF-κB signaling pathway in rats with Crohn's disease

Abstract

OBJECTIVETo observe the effect of stimulating Qihai (CV 6) and bilateral Tianshu (ST 25) with herb-partitioned moxibustion (HPM) in rats with Crohn's disease (CD), and to investigate the possible anti-inflammatory mechanism of HPM. METHODSForty rats were randomly divided into four groups (n = 10 rats per group): normal control (NC), model control (MC), mesalamine (MES), and HPM. The CD rat model was established in the MC, MES, and HPM groups by administering a mixture of trinitrobenzenesulfonic acid and alcohol via enema. The HPM group received HPM on Qihai (CV 6) and bilateral Tianshu (ST 25), while the MES group received intragastric mesalamine. Colonic histomorphological scores, and serum concentrations of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were assessed to evaluate the effects of HPM on colonic reparation and anti-inflammation. The expressions of Toll-like receptor 4 (TLR-4), nuclear factor κB inhibitor α (IkB-α), IkB kinase α/β (Iκκα/β), and NF-κB p65 were further analyzed to investigate the regulatory effects of the interventions on the TLR4/NF-κB pathway. RESULTSCD rats showed inflammatory colonic damage and increased serum concentrations of TNF-α and IL-1β. The expressions of TLR4, IKKα/β, and NF-κB p65 in the colons of CD rats were significantly increased compared with the NC group, while the expression of IκBα (a key negative regulator of NF-κB p65) was decreased. HPM significantly mitigated colonic damage and reduced the serum concentrations of TNF-α and IL-1β. HPM downregulated the expressions of TLR4, IKKα/β, and NF-κB p65 in the colon, and upregulated the expression of IκBα. The effects of HPM in CD rats were similar to those of mesalamine. CONCLUSIONHPM alleviates colonic inflammation in CD rats. This may be achieved through regulation of TLR4, which induces NF-κB signal transduction.