Inflammatory bowel disease refers to a group of non-specific chronic gastrointestinal inflammatory diseases of unknown causes, including ulcerative colitis, Crohn′s disease and indeterminate colitis.Recently, the incidence of inflammatory bowel disease in children has increased, which seriously affects the growth and development of children and the quality of life.Studies have shown that the opioid receptor antagonist naltrexone can reverse the inflammatory activity in inflammatory bowel disease and promote cell repair.This review summarized the research of application of naltrexone in the treatment of inflammatory bowel disease, aiming to further explore the effectiveness and safety of naltrexone in the treatment of inflammatory bowel disease in children.

Objective To evaluate the effects of different administration routes of lipid emulsion on bupivacaine-induced cardiotoxicity in rats.Methods Forty-eight clean healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 6 groups (n=8 each) using a random number table:Ⅳ infusion of normal saline (NS) group (group VN),Ⅳ infusion of lipid emulsion group (group VL),duodenal infusion of NS group (group DN),duodenal infusion of lipid emulsion group (group DL),intraperitoneal intusion of NS group (group PN) and intraperitoneal infusion of lipid emulsion group (group PL).In VN and VL groups,preheated NS and 20％ lipid emulsion 3 ml · kg-1 · min-1 were infused via the femoral vein for 5 min,respectively,and then 0.75％ bupivacaine was infused at the rate of 2 mg · kg-1 · min-1 until cardiac arrest happened.Preheated NS and 20％ lipid emulsion 15 ml/kg were infused via the duodenum (over 1 min,at a constant rate) in DN and DL groups,respectively,and were intraperitoneally infused in PN and PL groups,respectively,followed by an infusion of 0.2 ml/min for 15 min in DN,DL,PN and PL groups.Then 0.75％ bupivacaine was infused via the left femoral vein at a rate of 2 mg · kg-1 · min-1 until cardiac arrest happened.The time to ventricular arrhythmia,mean arterial pressure (MAP) decreasing to 50％ of the baseline and cardiac arrest was recorded.The amount of bupivacaine consumed was calculated immediately after ventricular arrhythmia occurred (T0),immediately after MAP decreased to 50％ of the baseline (T1) and immediately after occurrence of cardiac arrest (T2).Arterial blood samples were collected at T0-2 for determination of the concentration of bupivacaine in plasma by high-performance liquid chromatography.Results Compared with group VN,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly prolonged,and the amount of bupivacaine consumed was increased at T0-2 in group VL (P＜0.01).There was no significant difference in the parameters mentioned above between group DN and group DL,and between group PN and group PL (P＞0.05).Compared with group VL,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly shortened,and the amount of bupivacaine consumed was decreased at T0-2 in DL and PL groups (P＜0.01).Compared with group DL,the time to ventricular arrhythmia,MAP decreasing to 50％ of the baseline and cardiac arrest was significantly prolonged,and the amount of bupivaeaine consumed was increased at T0.2 in group PL (P＜0.05).There was no significant difference in the concentration of plasma bupivacaine between six groups (P＞0.05).Conclusion Ⅳ infusion of lipid emulsion can decrease bupivacaine-induced cardiotoxicity when compared with duodenal and intraperitoneal infusion in rats.

Objective:To investigate the protective effect of water-soluble dietary fiber fructooligosaccharides(FOS) on intestinal mucosal barrier in mice with ulcerative colitis(UC), and to find a new drug option for the treatment of patients with UC.Methods:This study used 4% dextran sodium sulfate(DSS)to induce a 7-day UC mouse model.Male C57BL/6 mice aged 6-8 weeks were randomly divided into three groups: the control group drank distilled water; The model group was given 4% DSS; The oligofructose group was administered 20 mg/mL FOS by gavage simultaneously with DSS induction.The body weight, fecal characteristics, and fecal blood status of mice daily, and the disease activity index(DAI)score were monitored.After the experiment, HE staining was used to observe the pathological changes in the colon tissue of mice.Real time fluorescence quantitative PCR, Western Blot, and immunofluorescence staining were used to detect the expression levels of tight junction proteins ZO-1, Claudin-1, and Occludin in the intestines of each group of mice.Results:Compared with control group, the weight of mice decreased and the DAI score increased in model group( P<0.05). However, the weight of mice in FOS group was higher than that in model group, and the DAI score was lower than that in model group ( P<0.05). Compared with control group, the colon length of mice in model group was shortened[(7.52±0.41)cm vs.(5.48±0.19)cm], and the histopathological score was increased (0.53±0.38 vs.3.51±0.18). However, the colon length of mice in FOS group[(6.82±0.63)cm] was longer than that in model group, and the hispathological score(2.33±0.63) was lower than that in model group.All the differences were statistically significant ( P<0.05). The expression levels of ZO-1, Claudin-1, Occludin protein and its mRNA levels in model group were lower than those in control group ( P<0.05). However, those of FOS group were higher than those in model group ( P<0.05). Conclusion:FOS could alleviate the symptoms of weight loss in UC mice, reduce their DAI score, improve inflammation of colon tissue, upregulate the expression of tight junction proteins ZO-1, Claudin-1, and Occludin, and protect the intestinal mucosal barrier.

Objective:To investigate the protective role of Yes-associated protein(YAP)in intestinal epithelial barrier injury.Methods:The intestinal epithelial barrier model was established by culturing human colorectal adenocarcinoma cell line Caco-2 cells, which were divided into four groups: control group, Caco-2 monolayers did not receive any treatment; recombinant human tumor necrosis factor-α(rhTNF-α)group, 100 μg/L of rhTNF-α was added to Caco-2 monolayers; vector+ rhTNF-α group, Caco-2 monolayers were first added with control plasmid pcDNA3.1-vector, and 100 μg/L rhTNF-α was added 24 hours later; YAP+ rhTNF-α group, Caco-2 cells with barrier construction were first added with pcDNA3.1-YAP, and 100 μg/L rhTNF-α was added 24 hours later.Realtime-PCR and Western blot were used to evaluate YAP mRNA and protein expression level.Epithelial permeability was assayed by trans-epithelial electrical resistance(TEER)and fluorescein isothiocyanate-dextran 40(FD-40 flu). Cellular distribution of F-actin was assayed by immunofluorescence staining.Results:Compared with control group[(607.3±29.3)Ω·cm 2], TEER of rhTNF-α group[(265.3±32.7)Ω·cm 2] decreased, while TEER of YAP+ rhTNF-α group[(387.0±18.7)Ω·cm 2]increased compared with rhTNF-α group, the differences were statistically significant( P<0.001). The FD-40 flux of rhTNF-α(22.7%±0.5%) group was higher than that of the control group(6.3%±0.9%), while the FD-40 flux of Yap + rhTNF-α group(12.2%±0.8%) was lower than that of rhTNF-α group, the differences were statistically significant( P<0.001). Immunofluorescence staining showed that compared with the control group, the cytoskeletal F-actin fiber dense spot decreased in rhTNF-α group, and some cells showed obvious trans-cellular stress fiber structure, while the peripheral actin band was clear in YAP+ rhTNF-α group, and the intracellular stress fiber decreased.YAP+ TNF-α group appeared as a clear, peripheral actin ribbon with a decrease in cytoplasmic stress fibres. Conclusion:YAP overexpression significantly inhibits TNF-α induced decline of TEER, and increases of FD-40 flux and F-actin rearrangement of Caco-2.YAP could ameliorate TNF-α induced intestinal epithelial barrier injury by regulating cytoskeleton F-actin.