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

OBJECTIVE
To 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.


METHODS
Forty 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 ¦Á (TNF-¦Á) and interleukin 1¦Â (IL-1¦Â) 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 ¦ÊB inhibitor ¦Á (I¦ÊB-¦Á), I¦ÊB kinase ¦Á/¦Â (IKK¦Á/¦Â), and NF-¦ÊB p65 were further analyzed to investigate the regulatory effects of the interventions on the TLR4/NF-¦ÊB pathway.


RESULTS
CD rats showed inflammatory colonic damage and increased serum concentrations of TNF-¦Á and IL-1¦Â. The expressions of TLR4, IKK¦Á/¦Â, and NF-¦ÊB p65 in the colons of CD rats were significantly increased compared with the NC group, while the expression of I¦ÊB¦Á (a key negative regulator of NF-¦ÊB p65) was decreased. HPM significantly mitigated colonic damage and reduced the serum concentrations of TNF-Î± and IL-1¦Â. HPM downregulated the expressions of TLR4, IKK¦Á/¦Â, and NF-¦ÊB p65 in the colon, and upregulated the expression of I¦ÊB¦Á. The effects of HPM in CD rats were similar to those of mesalamine.


CONCLUSION
HPM alleviates colonic inflammation in CD rats. This may be achieved through regulation of TLR4, which induces NF-¦ÊB signal transduction.