ABSTRACT
Objective To investigate the effects of enteral ecological nutrition on intestinal immune function and Hh protein expression in intestinal mucosa of rats with small intestinal injury and explore the mechanism. Methods Thirty male clean grade Wistar rats were selected as study subjects. The rats were randomly divided into a model group and an enteral ecotrophic group with 15 rats in each group. The small intestinal injury model was prepared by trauma method. After successful modeling, Six hours after successful establishment of the model, the rats in the two groups were fed with 753.12 kJ·kg-1·d-1 energy, 3 times a day. The rats in the model group were fed with conventional diet, while the rats in the enteral ecotrophic group were fed with enteral nutrition emulsion +Lactobacillus, bifidobacterium triple viable bacteria by intragastric administration of 1×107 cfu/d. After 10 days, the rats were killed, the small intestine of the two groups was dissected and stained with hematoxylin-eosin (HE) staining, and the morphological changes of small intestinal mucosa (villus height, glandular recess depth, mucosal thickness) were observed in the two groups; the expressions of CD3+, CD4+, CD8+ positive T cells in small intestinal mucosa were evaluated by immunohistochemistry; the expression of Hh protein in small intestinal mucosa was detected by Western Blot in the two groups. Results On the first day after the establishment of the model, the weight of rats in both groups was lower than that before the modeling [model group (g): 118.0±4.2 vs. 121.7±5.2, enteral ecotrophic group (g):117.5±4.7 vs. 120.8±5.0, P > 0.05], from the fifth day after the modeling, the weight of the rats in the enteral ecotrophic group was significantly higher than that of the model group (g: 127.1±5.0 vs. 123.2±4.2, P < 0.05), continued to 10 days (g: 142.5±6.6 vs. 135.3±6.2, P < 0.05). After the establishment of the model for 10 days, the small intestinal villus height, glandular recess depth, mucosal thickness and percentages of CD3+, CD4+ and CD8+ positive T cells in enteral ecotrophic group were significantly higher than those in model group [villus height (μm): 221.7±25.0 vs. 159.5±20.8, glandular recess depth (μm): 79.39±12.65 vs. 67.87±7.79, mucosal thickness (μm): 254.7±51.8 vs. 209.0±27.2, CD3+: 0.193±0.035 vs. 0.125±0.031, CD4+: 0.130±0.027 vs. 0.104±0.015, CD8+: 0.165±0.026 vs. 0.137±0.027, all P < 0.05]. The expression of Hh protein in the enteral ecotrophic group was obviously higher than that in model group (Hh/β-actin: 0.16±0.04 vs. 0.04±0.02, P <0.05). Conclusion Enteral ecological nutrition may promote the repair of intestinal mucosa and the improvement of immune function level by enhancing the expression of Hh protein in small intestinal mucosa of rats with small intestinal injury.
ABSTRACT
BACKGROUND/AIMS: DA-6034 has anti-inflammatory activities and exhibits cytoprotective effects in acute gastric injury models. However, explanations for the protective effects of DA-6034 on intestinal permeability are limited. This study sought to investigate the effect of DA-6034 on intestinal permeability in an indomethacin-induced small intestinal injury model and its protective effect against small intestinal injury. METHODS: Rats in the treatment group received DA-6034 from days 0 to 2 and indomethacin from days 1 to 2. Rats in the control group received indomethacin from days 1 to 2. On the fourth day, the small intestines were examined to compare the severity of inflammation. Intestinal permeability was evaluated by using fluorescein isothiocyanate-labeled dextran. Western blotting was performed to confirm the association between DA-6034 and the extracellular signal-regulated kinase (ERK) pathway. RESULTS: The inflammation scores in the treatment group were lower than those in the control group, but the difference was statistically insignificant. Hemorrhagic lesions in the treatment group were broader than those in the control group, but the difference was statistically insignificant. Intestinal permeability was lower in the treatment group than in the control group. DA-6034 enhanced extracellular signal-regulated kinase expression, and intestinal permeability was negatively correlated with ERK expression. CONCLUSIONS: DA-6034 may decrease intestinal permeability in an indomethacin-induced intestinal injury model via the ERK pathway.