| Objective:Acute gastrointestinal mucosal injury refers to the occurrence of acute mucosal erosion,bleeding or ulcers in the gastrointestinal mucosa under the state of stress(patients are subjected to various major operations and wounds,burns,cerebrovascular accidents,multiple organ failure,myocardial infarction,strong stimulation of hormones,non-steroidal anti-inflammatory and analgesic drugs).Lesions may involve the entire digestive tract,with gastroduodenal lesions being more common.The main clinical manifestations are hematemesis and melena.In severe cases,hematemesis may occur,and death may result from circulatory failure and shock.Intestinal tract is one of the most important digestive and immune organs in the human body,and intestinal mucosa plays a protective role by preventing intratuminal toxic substances and pathogenic bacteria from invading the body through a complex physiological mechanism.The mucus layer secreted by intestinal epithelial cells mainly composed of goblet cells is the first barrier to the contact of intestinal contents and plays the most important role.The secreted mucin MUC2 is the main component of intestinal mucus.To investigate the therapeutic effect of L-citrate on acute intestinal mucosal injury induced by dextran sulfate sodium(DSS)in mice and its possible mechanism.By observing the changes of the histology of lower goblet cells and the expression of MUC2 mucin in the mouse model of acute intestinal injury induced by dextran sulfate sodium(DSS),the therapeutic effect of L-citrulline was further confirmed,which could provide reference for the nutritional treatment and prevention of complications in patients with severe intestinal mucosal injury.Methods: After being established acute intestinal injury model,mice were randomly divided into experimental group and control group and blank control group,blank control group in the building after the completion of the abdominal cavity after intraperitoneal anesthesia,the experimental group and control group respectively to be 1(m L/d)5% of the L-citrulline and L-alanine continuous lavage in lavage 1,4,7,14 d after 12 h after the next day on an empty stomach in the abdominal cavity after anesthesia,respectively to extract 1 cm tissue of ileum,the proximal and distal colon rectum tissues,formaldehyde fixed specimens respectively after AB-PAS staining to observe intestinal epithelial morphology,immunohistochemical observation MUC2 expression quantity,Western blot was used to detect the expression of MUC2 after homogenation and hypercentrifugation.Results: Severe gastrointestinal symptoms involving hematochezia and hematemesis began to appear in DSS-induced acute intestinal injury model mice on the second day after intervention.In the experimental group,symptoms were significantly relieved on the second day after drug intervention,while there was no significant change in the control group.The body weight of the experimental group was significantly higher than that of the control group(P<0.05).The morphological structure of intestinal epithelium in the experimental group was better than that in the control group.Under the condition of acute intestinal injury,the expression level of MUC2 protein was significantly decreased,the highest expression level was observed on the 1st day after L-citrate intervention,and the expression level was decreased on the 4th day compared with the1 st day after L-citrulline intervention,and there was no significant difference in the expression level on the 7th and the 14 th day(P<0.05).Conclusion: L-citrulline for acute intestinal injury condition and function of intestinal mucosa epithelial cells in mice to restore has a promoting effect,and prove the Lcitrulline in the acute phase of intestinal injury can significantly reduce the mortality and improve the quality of survival,strengthen the close connection between intestinal epithelial cells,promote the intestinal mucosa mucus secretion,but acute period of MUC2 protein expression was not obviously promoted,this may indicate goblet cells secrete MUC2 mucin may be a self-limited recovery process. |