Study on the bifidobacterial adhesion to the host tissue in ulcerative colitis and related serum inflammatory factors with Pingkui enema / 国际中医中药杂志

ABSTRACT

Objective This study is designed to investigate the effect and mechanism of Pingkui enema in treatment of ulcerative colitis. Methods Sixty SD rats at SPF level were randomly divided into 6 groups which were normal group, model group, and the low, medium and high dose groups of Chinese medicine Pingkui enema, and sulfasalazine (SASP) enema group. The normal group and model group were given an equal volume of saline enema after modeling. After continuous administration for 10 days, the histopathological effects were evaluated after extraction, and the serum interleukin-8 (IL-8), interleukin-13 (IL-13), tumor necrosis factor (TNF-α), rat intestinal mucosal bifidobacteria adhesion and adhesin receptor were measured by enzyme-linked immunosorbent assay (ELISA). The real-time fluorescence quantitative PCR (RT-PCR) were used to detect the intestinal bifidobacterial content. Results Compared with the model group, the content of IL-8 (153.50 ± 8.59 pg/ml, 150.84 ± 5.38 pg/ml vs. 167.13 ± 13.66 pg/ml), TNF-α (330.08 ± 10.02 pg/ml, 287.27 ± 13.89 pg/ml vs. 376.50 ± 19.06 pg/ml) in medium, high dose group of Pingkui enema significantly decreased (P<0.05), while the IL-13 (37.04 ± 3.62 pg/ml, 40.64 ± 5.98 pg/ml vs. 31.57 ± 2.95 pg/ml) significantly increased (P<0.05). The bifidobacteria adhesin (124.84 ± 9.74 ng/L, 149.93 ± 9.57 ng/L, 176.74 ± 11.01 ng/L vs. 101.11 ± 17.18 ng/L) and adhesin receptor (78.44 ± 14.03 ng/L, 99.50 ± 3.63 ng/L, 107.36 ± 5.05 ng/L vs. 60.96 ± 13.89 ng/L) in low-, medium-, high dose group of Pingkui enema significantly increased (P<0.05). The content of bifidobacteria (1 331.4 ± 242.2 copies/μl vs. 490.5 ± 106.0 copies/μl) in the middle dose Pingkui enema group significantly increased (P<0.05). Conclusions The Pingkui enema can promote the colonization of intestinal epithelial cells by promoting bifidobacteria, increase bifidobacterium adhesin and adhesin receptors, up-regulate the expression of IL-13, and down-regulate the expression of IL-8, TNF-α.