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1.
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care ; (6): 275-278, 2019.
Article in Chinese | WPRIM | ID: wpr-754554

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.

2.
Acta Anatomica Sinica ; (6)2002.
Article in Chinese | WPRIM | ID: wpr-572659

ABSTRACT

Objective To establish a model of injury to primarily cultured spinal cord neurons,mimicking the neuronal injury after complete transactional spinal cord trauma,for the sake of exploring changes in expression of an immediately-early gene,c-jun,in central nervous system injury. Methods Spinal cords were removed form fetal Wistar rats at the 14th gestation day and the neurons were cultured for 10 to 12 days.Then,mechanical injury was applied to the neurons by making regular scores on the culture disk under direct vision with the aid of a self-made standard template.Morphology of the injured neurons and changes in expression of c-Jun protein were observed before and at different intervals after injury. Results c-Jun expression was noted in neuronal nuclei 10 min after injury and its peak appeared at 2 hrs.Besides,the density of positive neurons bore evidently an inverse proportion with their distance from the scores.Conclusion\ Positive expression in injury neurons show that c-jun gene enters the nucleoli of injured neurons and takes the role of “the third messenger” at early time after neuronal injury.

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