Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation

摘要

AIM To inve s t igat e t he t he r ape ut ic e f f e c t of Jianpi Qingchang decoction(JPQCD) on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC) in mice.METHODS C57BL/c mice were injected intragastrically with 5% DSS instead of drinking water for 7 d, and their body weight, diarrhea severity and fecal bleeding were monitored, while the mice in the control group were treated with standard drinking water, without DSS. After 7 d, the DSS drinking water was changed to normal water and the DSS group continued with DSS water. The control and DSS groups were given normal saline by intragastric injection. The 5-aminosalicylic acid(5-ASA) group was treated orally with 5-ASA at a dose of 100 mg/kg daily. The JPQCD group was treated orally with JPQCD at a dose of 17.1 g/kg daily. On day 14, the colon length was measured, the colorectalhistopathological damage score was assessed, and protein levels of interleukin(IL)-1β, IL-8 and tumor necrosis factor-alpha(TNF-α) in colon supernatants were measured by enzyme-linked immunosorbent assay. m RNA expression of IL-1β, IL-8, TNF-α and nuclear factor-kappa B(NF-κB) was detected by realtime quantitative polymerase chain reaction. Western blotting was used to detect the protein expression of NF-κB and inhibitor of kappa B. RESULTS Acute inflammation occurred in the mice administered DSS, including the symptoms of losing body weight, loose feces/watery diarrhea and presence of fecal blood; all these symptoms worsened at 7 d. The colons of mice treated with DSS were assessed by histological examination, and the results confirmed that acute inflammation had occurred, as evidenced by loss of colonic mucosa and chronic inflammatory cell infiltration, and these features extended into the deeper layer of the colon walls. The expression levels of IL-1β, IL-8 and TNF-α in the DSS group were higher than those in the control group(P 0.05). Comparing with the DSS group, due to using JPQCD and 5-ASA, significant suppression of activation in DSSinduced NF-κB and increased phosphorylation of IκB in mice with experimental colitis occurred(P 0.05). CONCLUSION Activation of the NF-κB signaling pathway is inhibited by JPQCD, which shows the potential mechanism by which JPQCD treats UC.