Effects of glutamine on intestinal permeability and bacterial translocation in TPN-rats with endotox

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:jingbao0804
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AIM:To evaluate the protective effect and mechanism ofglutamine on the intestinal barrier function in totalparenteral nutrition (TPN) rats with trauma or endotoxemia.METHODS:To perform prospective,randomized andcontrolled animal experimentation of rats with surgicaltrauma,TPN and endotoxemia,thirty-four male,adultSprague Dawley rats were divided into four groups:controlgroup (n=8),TPN group (n=-9),trauma and endotoxemiagroup (LPS,n=8) and trauma plus endotoxemiasupplemented with glutamine in TPN solution group (Gin.group,n=-9).All groups except the control group weregiven TPN solutions in 7-day experimental period.For Gingroup,1 000 mg/kg/d of glutamine was added to TPNsolution during day 1-6.On the 7th day all the animalswere gavaged with lactulose (66 mg) and mannitol (50 mg)in 2 ml of normal saline.Then 24 h urine with preservativewas collected and kept at -20℃.On day 8,under intra-peritoneal anesthesia using 100 mg/kg ketamin,theintestine,liver,mesenteric lymph nodes and blood weretaken for examination.RESULTS:The body weight of LPS group decreased mostamong the four groups.The structure of small intestinalmucosa in TPN group,LPS group and Gin group showedimpairments of different degrees,and the damage of smallintestinal mucosa in Gin group was remarkably alleviated.The concentrations of interleukins in small intestine mucosawere lower (for IL-4 and IL-6) or the lowest (IL-10) in Gingroup.The IgA level in the blood plasma and the mucosaof Gin group was the highest among all of the groups.Theurine lactulose/mannitol test showed that the intestinalpermeability in LPS group was lower than that in TPN group(P<0.001),but there was no difference between LPS groupand Gin group.The rate of bacterial translocation in Gingroup was lower than that in LPS group (P<0.02).CONCLUSION:Prophylactic treatment with glutaminecould minimize the increments of intestinal permeabilityand bacterial translocation caused by trauma andendotoxemia in rats treated with TPN. AIM: To evaluate the protective effect and mechanism of glutamine on the intestinal barrier function in total parenteral nutrition (TPN) rats with trauma or endotoxemia. METHODS: To perform prospective, randomized and controlled animal experimentation of rats with surgical trauma, TPN and endotoxemia, thirty-four male , adult Sprague Dawley rats were divided into four groups: controlgroup (n = 8), TPN group (n = -9), trauma and endotoxemia group (LPS, n = 8) and trauma plus endotoxemiasupplemented with glutamine in TPN solution group , n = -9). All groups except the control group were given TPN solutions in 7-day experimental period. For Gingroup, 1000 mg / kg / d of glutamine was added to TP Nsolution during day 1-6.On the 7th day all the animals were gavaged with lactulose (66 mg) and mannitol (50 mg) in 2 ml of normal saline. After 24 h urine with preservativewas collected and kept at -20 ° C. On day 8, under intra-peritoneal anesthesia using 100 mg / kg ketamin, theintestine, liver, mesenteric lymph nodes and blood we retaken for examination .RESULTS: The body weight of LPS group decreased mostamong the four groups. The structure of small intestinal mucosa in TPN group, LPS group and Gin group showed impments of different degrees, and the damage of small intestinal mucosa in Gin group was remarkably alleviated. The concentrations of interleukins in small intestine mucosawere lower (for IL-4 and IL-6) or the lowest (IL-10) in Gingroup. IgA level in the blood plasma and the mucosaof Gin group was the highest among all of the groups Theurine lactulose / mannitol test showed that the intestinal permeability in LPS group was lower than that in TPN group (P <0.001), but there was no difference between LPS group and Gin group. Rate of bacterial translocation in Gingroup was lower than that in LPS group (P <0.02) .CONCLUSION: Prophylactic treatment with glutaminecould minimize the increments of intestinal permeability and bacterial translocation caused by trauma andendotoxemia in rats treated with TPN.
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