Experimental Study on the Treatment of Ulcerative Proctitis in Rats by Combining Baitouweng Decoction with Mesalamine Retention Enema

Abstract

To study the effect and mechanism of Baitouweng decoction, mesalamine and its combination with an enema in the treatment of ulcerative proctitis in rats is the objective of the study. The rats were divided into seven groups: Control (Normal), model (ulcerative proctitis), mesalamine, Baitouweng decoction, lowdose Baitouweng decoction combined with mesalamine, medium-dose Baitouweng decoction combined with mesalamine, high-dose Baitouweng decoction combined with mesalamine group. Except for the control group, all rats were induced with a 5 % acetic acid solution for ulcerative proctitis. The severity of ulcerative proctitis was measured by the disease activity index score; morphological changes of rectal tissue were observed by hematoxylin and eosin staining; expression of cytokines tumor necrosis factor alpha, interleukin-1 beta, interleukin-6, interferon‐gamma, interleukin-10 messenger ribonucleic acid was detected by reverse transcription-polymerase chain reaction; Western blot analysis of signaling pathway proteins nuclear factor kappa B p65 and phosphorylated-nuclear factor kappa B p65 and the expression of tight junction proteins claudin-1, occludin and zonula occludens-1 was detected by Western blot and immunohistochemistry. The results revealed that the disease activity index scores of rats in each dosing group were significantly lower than those in the ulcerative proctitis group. After treatment, the expression of pro-inflammatory factors tumor necrosis factor alpha, interleukin-1 beta, interleukin-6 and interferon‐gamma was inhibited and the expression of the anti-inflammatory factor interleukin-10 was up-regulated. In conclusion, Baitouweng decoction combined with mesalamine had a synergistic effect on the treatment of ulcerative proctitis. The mechanism of action may be to regulate the synthesis and release of inflammatory factors by inhibiting the over-activation of nuclear factor kappa B p65, reducing the damage of pro-inflammatory factors to rectal mucosa and repairing the intercellular tight junction structure, thus improving the intestinal barrier and reducing the rectal inflammatory response.