Abstract
BackgroundHerb-partitioned moxibustion (HPM) at Tianshu (ST25) and Qihai (RN6) has been used to treat Crohn’s disease (CD). Injury to intestinal epithelial tight junctions (TJs) is the leading cause of CD onset with under expression of TJ-related proteins such as occludin, claudin-1, and zonula occludens protein-1 (ZO-1). This study aimed to investigate whether HPM can change the permeability of the intestinal epithelial barrier by affecting the expression of colonic epithelial TJ-related proteins in vitro.MethodsForty-eight male Sprague–Dawley rats were randomly divided into four groups of twelve rats: normal control (NC) group; model control (MC) group; herb-partitioned moxibustion (HPM) group; and mesalazine control (MESA) group. The rats in the latter three groups were given trinitrobenzene sulfonic acid (TNBS) enemas to establish CD models. The HPM group was treated with HPM at Tianshu (ST25) and Qihai (RN6) once daily for 14 consecutive days, while the MESA group was given mesalazine solution (at the proportion of 0.018:1) by lavage twice daily for the same period. After the treatment period, the colon tissues from all groups were partly processed for macroscopic damage assessment and histological observation, and partly purified and cultured in vitro to examine the permeability of the intestinal epithelial cell barrier by trans-epithelial electrical resistance (TEER). Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR) analyses were performed to observe the expression of occludin, claudin-1, and ZO-1 proteins and mRNAs, respectively.ResultsIn the HPM and MESA groups, the typical CD macroscopic damage, i.e., inflammatory cell infiltration in colonic mucosa and submucosa, submucosal lymphoid follicular hyperplasia, hyperemia and edema, and morphological changes were improved to different degrees in the colonic tissues (HPM, MESA vs. MC for macroscopic score of colonic damage: all P < 0.001). The decreasing tendencies were minor for colonic TEER values (HPM, MESA vs. MC: all P < 0.001), and expression of intestinal epithelial TJ-related proteins (HPM, MESA vs. MC: all P < 0.05) and mRNAs (HPM, MESA vs. MC: all P < 0.05), especially in the HPM group (HPM vs. MESA for TEER values: P < 0.001).ConclusionsHPM at Tianshu (ST25) and Qihai (RN6) upregulated the expression of occludin, claudin-1, and ZO-1 in TNBS-induced CD model rats.Electronic supplementary materialThe online version of this article (doi:10.1186/s13020-016-0090-0) contains supplementary material, which is available to authorized users.
Highlights
Herb-partitioned moxibustion (HPM) at Tianshu (ST25) and Qihai (RN6) has been used to treat Crohn’s disease (CD)
Expression of occludin, claudin‐1, and ZO‐1 proteins in the different groups For occludin protein expression (Fig. 4a), there was a significant decrease in the model control (MC) group compared with the normal control (NC) group (P = 0.000), significant increases in the HPM and mesalazine control (MESA) groups compared with the MC group (P = 0.025, P = 0.019), and no significant difference between the HPM group and the MESA group (P = 0.859), but significant differences in the HPM and MESA groups compared with the NC group (P = 0.001, P = 0.000)
For claudin-1 protein expression (Fig. 4b), there was a significant decrease in the MC group compared with the NC group (P = 0.000), significant increases in the HPM and MESA groups compared with the MC group (P = 0.001, P = 0.002), no significant difference between the HPM group and the MESA group (P = 0.535), and no significant differences in the HPM and MESA groups compared with the NC group (P = 0.196, P = 0.073)
Summary
Herb-partitioned moxibustion (HPM) at Tianshu (ST25) and Qihai (RN6) has been used to treat Crohn’s disease (CD). Injury to intestinal epithelial tight junctions (TJs) is the leading cause of CD onset with under expression of TJ-related proteins such as occludin, claudin-1, and zonula occludens protein-1 (ZO-1). This study aimed to investigate whether HPM can change the permeability of the intestinal epithelial barrier by affecting the expression of colonic epithelial TJ-related proteins in vitro. Malformation and dysfunction of intestinal epithelial TJs were found in patients with IBDs [6, 7], and related to under expression or abnormal distribution of intestinal epithelial TJ-related proteins [8]. During active and non-active periods of CD, the expression of occludin, claudin-1, ZO-1 proteins and mRNAs were significantly reduced in the colonic mucosa, followed by increasing permeability of the intestinal epithelium and injury to the intestinal epithelial barrier [13, 14]
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