Objective To study the effect of glutamine (Gln) on the intestinal mucosa inflammatory reaction and permeability after intestine ischemia-reperfusion injury in rats.Methods The rat model of intestinal ischemia-reperfusion injury was established by clamping the mesenteric superior artery and then restoring blood flow.Forty-eight model rats were divided into control group (n =24) and model + Gln group (n =24)according to the stochastic indicator method.Both groups were given enteral nutrition with equal energy and nitrogen [energy 125.4 kJ/ (kg · d) and nitrogen 0.2 g/ (kg · d)].The model +Gln group was fed with enteral nutrition plus 3％ Gln,while the control group was fed with enteral nutrition plus 3％ soybean protein.The experiment lasted 8 days after modeling.The intestinal mucosa and the plasma levels of nuclear factor-κB (NF-κB),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),Gln,D-LACtic acid and diamine oxidase (DAO) were observed in rats before and after modeling and on the 3rb and 8rd day of the experiment.Changes in the morphology of intestinal mucosa were observed by electron microscopy.Results After modeling in control and model + Gln group,the level of NF-κB in intestinal mucosa [18 cases (75.0％) and 17 cases (70.8％)] were significantly higher than those before modeling [0 case (0.0％),P =0.013,P =0.019],the level of IL-6 in intestinal mucosa [(313.27±75.28) pg/g and (321.75±76.46) pg/g] were significantly higher than those before modeling [(227.52 ±58.13) pg/g,P =0.023,P =0.043],and the level of TNF-α in intestinal mucosa [(241.28 ±65.29) pg/g and (240.35 ±64.86) pg/g] were significantly higher than those before modeling [(172.45 ±33.76) pg/g,P=0.036,P=0.011].The plasma level of IL-6 [(150.32 ± 18.74) ng/L and (148.21 ±20.19) ng/L] were significantly higher than those before modeling [(116.37 ± 14.59) ng/L,P =0.032,P =0.025],the plasma level of TNF-α [(127.62 ± 14.24) ng/Land (123.86 ± 13.75) ng/L] were significantly higher than those before modeling [(85.18 ± 8.84) ng/L,P =0.018,P =0.035],and the plasma level of D-LAC [(0.46 ±0.03) mmol/L and (0.51 ±0.04) mmol/L]were significantly higher than those before modeling [(0.27 ±0.02) mmol/L,P =0.041,P =0.018],and the plasma level ofDAO [(2.76±0.57) U/ml and (2.58 ±0.51) U/ml] were significantly higher than those before modeling [(1.52±0.24) U/ml,P=0.015,P=0.037],while the plasma level of Gln [(0.18 ±0.01) g/L and (0.21 ± 0.01) g/L] were significantly lower than those before modeling [(0.39 ± 0.03) g/L,P =0.026,P =0.031].On the 3rd and 8th days of the experiment in the control group,the level of NF-κB in intestinal mucosa [16 cases (66.7％),15 cases (62.5％)] were significantly higher than those before modeling (P =0.027,P =0.002),the level of TNF-α in intestinal mucosa [(226.23 ±55.35) pg/g and (214.76 ±54.82) pg/g] were significantly higher than those before modeling (P=0.042,P =0.038)],the level of IL-6in intestinal mucosa [(297.56 ± 71.39) pg/g and (291.49 ± 68.46) pg/g] were significantly higher than those before modeling (P =0.031,P =0.012).On the 3rd and 8th days in the control group,the plasma level of IL-6[(147.38 ± 17.25) ng/L and (144.65 ± 15.32) ng/L] were significantly higher than those before modeling (P =0.016,P =0.034),the plasma level of TNF-α [(121.75 ± 13.72) ng/L and (113.83 ± 11.69) ng/L] were significantly higher than those before modeling (P =0.025,P =0.041),the plasma level of D-LAC [(0.41 ±0.03) mmol/L and (0.53 ±0.05) mmol/L)] were significantly higher than those before modeling (P =0.029,P =0.030),the plasma level of DAO [(2.51 ± 0.52) U/ml and (1.76 ± 0.34) U/ml] were significantly higher than those before modeling (P =0.034,P =0.016).The plasma level of Gln [(0.22 ±0.01) g/L and (0.21 ±0.03) g/L] were significantly lower than those before modeling (P =0.042,P =0.035).On the 3rd day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [14 cases (58.3％),(213.78 ±43.76) pg/g,(293.72 ±69.86) pg/g] were significantly higher than those before modeling (P =0.038,P =0.026,P =0.013) ; the plasma level of IL-6,TNF-α,D-LAC,and DAO [(135.61 ±14.25) ng/L,(117.35 ±11.29) ng/L,(0.45 ±0.03) mmol/L,and (2.26 ± 0.43) U/ml] were significantly higher than those before modeling (P =0.021,P =0.032,P =0.032,P =0.025).On the 8th day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [9 cases (37.5％),(184.53 ± 42.16) pg/g,and (236.83 ±66.52) pg/g] were significantly lower than those after modeling and those in the control group (P =0.024,P=0.027; P=0.026,P=0.039; P=0.013,P=0.028) ; the plasma levels of IL-6,TNF-α,D-LAC,and DAO [(126.35±12.74) ng/L,(92.76±9.42) ng/L,(0.31 ±0.02) mmol/L,and (1.76±0.34) U/ml]were significantly lower than those after modeling and those in the control group (P =0.021,P =0.030; P =0.032,P =0.025 ; P =0.024,P =0.037 ; P =0.022,P =0.036) ; the plasma level of Gln [(0.40 ±0.03) g/L] was significantly higher than those after modeling and in the control group (P =0.028,P =0.032).Under the electron microscope,the structure of villus and recess was damaged after modeling,villi were sparse and short,with a lot of inflammatory cell infiltration in the lamina propria.Lymphangiectasia and edema occured after modeling.On the 8th day,compared with after modeling and the control group,intestinal villi and recess structure were significantly restored in the model + Gln group; compared with the after-modeling status,the recovery of intestinal mucosa villi and recess structure was not obvious,and the inflammatory cell infiltration in the lamina propria persisted in the control group.Conclusion Gln repairs ischemia-reperfusion injury in the intestinal mucosa by regulating intestinal mucosa inflammatory cytokine release,inhibitng inflammatory response,and reducing the permeability of the intestinal mucosa.