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"Bowel Disease Pulmonary" Effect On The Signal Pathway And Lung Intestinal Micro Ecology

Posted on:2015-08-23Degree:MasterType:Thesis
Country:ChinaCandidate:J Y XuFull Text:PDF
GTID:2284330467980601Subject:TCM clinical basis
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Objective:"Through the replication SD rat model of ulcerative colitis," synchronous observation treatment group, model group and blank group rat transforming in intestinal tissue at different time points in the lung growth factor and epidermal growth factor expression, at the same time looking for pulmonary and intestinal microecological flora changes, to explore the "lung and intestine pathological change" the mechanism and material basis, so as to provide a theoretical basis for "lung disease cure" method.Methods:100healthy SD rats were randomly divided into treatment group, model group and blank group, the model group except for40, the remaining two groups with30rats in each group. The rats in the model group and the treatment group (three rats with TNBS induced by trinitrobenzene sulphonic acid enema, construction of "ulcerative colitis" model, the blank control group rats were given normal saline enema. The first model was repeated every7days until the end of the experiment model. The rats in the treatment group at eighth days after gavage treatment, choose three decoction, the blank group and the model group rats according to the method given normal saline enema,1times a day. In the first model after eighth,29,50days, the rats were killed and the lung tissues of colon, HE staining to observe pathological changes, changes in electron microscopy ultrastructure, immunohistochemistry intestines, lung tissue expression of EGF/ErbB3and TGF β/TGF β R/Smads signal related proteins and detection of bacteria results.Result:1.Immunohistochemistry:The eighth day, decreased the expression of EGF/ErbB3protein in colon tissue of model group rats, the expression of TGFβ/TGFβR/Smads signal related protein increased significantly, the expression of EGF/ErbB3and TGFβ/TGFβR/Smads signal protein in lung tissue did not change significantly, model twenty-ninth,50days, the expression of EGF/ErbB3protein in colon tissue gradually increased, the expression of TGF the β/TGFβR/Smads signal related protein decreased gradually, the expression of EGF/ErbB3and TGFβ/TGFβR/Smads signal protein in lung tissue were significantly changed.Twenty-ninth days, the treatment group compared to the model group rats EGF/ErbB3signal protein expression was significantly increased, the expression of TGFβ/TGF P R/Smads signal related protein decreased, expression of EGF/TGF beta signaling protein in lung tissue were significantly increased, ErbB3/TGF P R/Smads signal protein expression did not change significantly; fiftieth days, the treatment group than those in the model group rats, EGF/ErbB3and TGFβ/TGFβR/Smads signal protein expression did not change significantly decreased; R protein expression of TGF in lung tissue, EGF/ErbB3and TGF/Smads signal protein expression did not change obviously2bacteria:Model eighth days, aerobic count and Staphylococcus synchronous increase in respiratory and intestinal, anaerobic count and Enterobacter increase and decrease in the gut in the respiratory tract. Model twenty-ninth days, total aerobic and Staphylococcus to reduce synchronization in the respiratory tract and intestinal tract, anaerobic count and Enterobacteriaceae decreased while increased in the intestinal tract in the respiratory tract; model fiftieth days, respiratory and intestinal aerobic, anaerobic and total number of Staphylococcus synchronous increase in respiratory tract and intestinal tract. Treatment twenty-ninth,50days, intestinal and respiratory Enterobacteriaceae and Clostridium perfringens synchronous increase at the same time, the treatment group compared with the model group, the total number of bacteria changed significantly, the treatment group of fiftieth days each strain test results with the control group no significant differencesConclusion:1"ulcerative colitis" rat model can appear lung injury, lung injury time lags behind the time of colonic lesions, and the degree of injury and associated with colonic lesion progression, bowel disease can affect the lung, the change is a gradual process of evolution.The expression of EGF/ErbB32in lung and gastrointestinal tissue correlated with specific:experimental study found that, lung and intestine of rat model of ulcerative colitis in the EGF/ErbB3 associated with the TGFβ/TGFβR/Smad signal protein changes, may guide "pathological bowel disease and lung" transfer process through the repair of injury induced on colon and lung, may be one of the "common basic material base of bowel disease and pulmonary pathological changes," lung and large intestine is realized by the related regulation of EGF/ErbB3and TGFβ/TGFβR/Smad in pathological conditions, to further prove the "lung and large intestine" can can.Change3"ulcerative colitis" treatment groups compared with model rats lung injury process related protein is more obvious, pharmacological intervention may have a positive effect on lung tissue injury repair process, at the same time that the colon tissue compared with lung injury occurs earlier, the repair process of short duration, the experimental performance more prominent, and the lung tissue repair completely need longer time.4from the microecological bacteria change point of view:in the presence of ulcerative colitis, lung intestinal flora can appear synchronous changes, or increase or reduce synchronization, synchronization. Description can be intestinal lesions and lung lesions, microflora changes may be "one of the ways and forms of bowel disease and pulmonary", drug intervention may have a positive effect on intestinal and respiratory tract flora adjustment process, provide part of the micro ecology experimental basis for "lung and large intestine".5through the intervention mechanism of drugs, cause changes in expression of lung gut associated signaling pathway protein and changes of microflora, provides a more scientific basis for "lung disease treatment".
Keywords/Search Tags:Lung and large intestine share exterior-interior relationships, chronicbronchitis, pulmonary disease affected large intestine, Transforming Growth Factor(TGF), Epidermal Growth Factor (EGF)
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