Based On The Bowel Diseases Pathological Changes Of Inflammatory Factors In Rats Model Of Change "Bowel Disease And Lung" Paghological Mechanism

Objective:The enteropathy (ulcerative colitis) animal model, based on the three different time points, observation of rat general behavior, pulmonary and gastrointestinal function, intestinal and lung tissue pathological changes and related inflammatory mediators(TNF-α、IL-1β PGE2) and other aspects of the corresponding changes exploration of " bowel disease, and pulmonary pathology transmission mechanism".Methods:In SD rats, male,60. Were randomly divided into the blank control group (24rats) and model group (36rats). All rats of conventional adaptive feeding after1weeks, the rats in the model group (TNBS construction three trinitrobenzene sulfonic acid) induced ulcerative colitis model rats; the blank control group according to the above method is given the same amount of normal saline enema. The first model after every7days according to the above method repeated molding, until the end of the experiment. Rats were observed spirit, eating, feces and weight. In the first model after8,29,50days before the rats were sacrificed, executed on rat pulmonary function, gastrointestinal function determination, were sacrificed after HE staining microscopic observation of lung, colon, heart, liver, spleen, Kidney Pathological changes. Electron microscopic observation of lung and colon tissue pathological morphology, and ELISA detection on the lung and colon tissue of TNF-α、IL-1β、PGE2content.Results:1Pulmonary and gastrointestinal function changesGastrointestinal function:compared with the blank group, model group rats8,29,50days of gastric residual rate increased significantly, showing significant difference (P<0.01); compared with the blank group, the rats in the model group eighth,29,50days of small intestinal propulsion rate was significantly reduced, showing significant difference (P<0.01);Pulmonary function:compared with the blank group, model group rats8,29,50days of respiratory frequency without significant change (P>0.05); the rats in model group were eighth,29,50days tidal volume was significantly reduced, showing significant difference (P<0.01); the rats in the model group eighth,29days per cent ventilation volume is reduced, a differential expression (P<0.05), fiftieth days was significantly reduced, showing significant difference (P<0.01).2Pathological Morphology2.1Then performance2.1.1model8,29,50days, the blank control group and model group rats heart, liver, spleen, kidney tissues were not obvious.2.1.2The rats in the model group of eighth days of colonic mucosal epithelial cell degeneration and necrosis, erosion, submucosa and muscularis inflammatory cell infiltration. Twenty-ninth days of colonic tissue mucosa with focal erosions, submucosal infiltration. In fiftieth days of atypical epithelial cells, has the characteristics of ulcer repair. The blank group of rat intestinal mucosal epithelial cells arranged in rows.2.1.3The rats in the model group of eighth days lung bronchiolar epithelium focal degeneration and necrosis, inflammatory cell infiltration, inflammatory exudate, epithelial cell shedding. Twenty-ninth days of lung tissue with focal epithelial cell degeneration and necrosis, within the lumen of the inflammatory exudation. Fiftieth days of lung tissue visible bronchial widespread or multifocal epithelial cell necrosis, loss, within the lumen of the inflammatory exudation blank rats showed no alveolar, bronchial injury.2.2Electron performance2.2.1Colon organization performance electron microscopyThe control group of bowel mucosa is smooth, gland mouth is clear, microvilli is in order. Model of eight days of bowel mucosa layer disappear, only remains of epithelial cells after necrotic tissue.29days microvilli some disappear, markedly swollen mitochondria, intravascular mononuclear cells increased, the inherent layer appeared red blood cells.50days epithelium cells of empty bubble, degeneration, necrosis, a lot of bacteria appear, with only the collagen fiber tissue, the mucous membrane cells become pyknotic, degeneration, inflammatory cells apart, and visible focal bleeding. 2.2.2the lung tissue performance electron microscopyThe control group visible structure is clear, the model of day8, mitochondria swelling obviously, a lot of red blood cells appear and visible within the nucleus a few empty bubble.29days pulmonary capillaries mononuclear cells in increasing, epithelial cell falls off, lost, the nucleus of empty bubble appear within50days lung mesenchymal cells less composition, mesenchymal cells inside a large empty bubble, endothelial cells markedly swollen mitochondria, Ⅱ type epithelial cells myoglobin fluff.3inflammatory mediatorsTNF-α, IL-1β, PGE2content change:compared with control group, model group rats model of eighth days, twenty-ninth days, fiftieth days of colon tissue, lung TNF-a, IL-1β, PGE2content increased significantly, and there was significant difference (P<0.01); and molding eighth days, model rats model of twenty-ninth days, fiftieth days of lung, colon tissue TNF-α, IL-1β, PGE2content increased significantly, and there was significant difference (P<0.01); and molding twenty-ninth days, the rats in the model group model fiftieth days lung, colon tissue TNF-α, IL-1β, PGE2content obviously, there was significant difference (P<0.01).Conclusion:1.Bowel disease rat can appear on the changes of pulmonary function and pulmonary pathological changes, prompting bowel disease may transfer to the" lung".2.The heart, liver, spleen, kidney function were not significantly altered, suggestive of lung and large intestine function in close contact.3.Preliminary findings in the colon and lung tissue in TNF-α、IL-1β、PGE2and other inflammatory mediators of the corresponding changes, which may be" bowel disease and lung " corporeal foundation.