Animals ; Chickens ; Cold Temperature ; adverse effects ; Gastric Mucosa ; metabolism ; pathology ; physiopathology ; Intestinal Mucosa ; metabolism ; pathology ; physiopathology ; Male ; Serum ; metabolism

OBJECTIVETo investigate the morphological changes in intestinal villi after severe burns in rats, so as to explore its possible relationship with enteral bacterial translocation.

METHODSFifty Wistar rats were employed in the study, 10 of them were assigned to the control group (C). The rest 40 rats were subjected to 30% TBSA full-thickness scalding (burn group, B). 4 ml/100 g normal saline was given intra-peritoneally to the injured rats. The changes of the caliber of the central chyliferous vessel, the intestinal water content and the mucosal morphology of the terminal ileum were determined in the rats in C group and in B group at 8, 12, 24 and 48 postburn hours. The morphology of villi was observed with scanning electron microscope and light microscope.

RESULTSThe ileal villi appeared normal in C group. The central chyliferous vessel dilated persistently in rats of B group at all postburn time points, and dilatation was more evident in B group compared with control group (P < 0.01). At the same time an abundant amount of lymph was observed in the central chyliferous vessel. The intestinal water contents decreased to (70.5 +/- 2.2)% and (69.5 +/- 3.1)% in rats of B group at 8 and 12 PBHs, respectively, and they were obviously lower than that in C group (76.9 +/- 1.5)%, (P < 0.01). The intestinal water content in B group was similar to that in C group at 24 and 48 PBH (P > 0.05).

CONCLUSIONThe morphological changes in the intestinal villi of rats with severe burn injury may predispose the invasion of enteral toxin and bacteria. Intestinal lymphatics can be an important route for enteral bacterial translocation. The water reabsorption of the intestinal mucosa can be transiently enhanced during early postburn stage.

Animals ; Burns ; metabolism ; pathology ; Intestinal Mucosa ; metabolism ; pathology ; Intestine, Small ; pathology ; Rats ; Rats, Wistar ; Thoracic Duct ; pathology

OBJECTIVETo explore the changes in the PGE(2) and PGI(2), TXA(2) levels and PGT mRNA expression in the intestinal mucosa in scalded rats.

METHODSWistar rats inflicted with TBSA 30% III degree scald were employed as the model. The PGE(2) and PGI(2) and TXA(2) contents in the intestinal mucosa were measured by radioimmunoassay, and the expression of PGT mRNA was detected by in situ hybridization.

RESULTSThe PGE(2) and PGI(2) levels in intestinal mucosa were increased at 12 postburn hours (PBHs) and thereafter decreased dramatically (P < 0.05). The TXA(2) level in intestinal mucosa of scalded rats was obviously higher than that of normal level at 24 and 48 PBHs (P < 0.05), and the expression of PGT mRNA seemed to be increased after scalding.

CONCLUSIONThe decrease of PGE(2) level and the increase of TXA(2) level in the intestinal mucosa of scalded rats might be involved in rat mucosal injury, and PGT played an important role in the regulation of PGs levels.

Animals ; Burns ; metabolism ; pathology ; Intestinal Mucosa ; metabolism ; pathology ; Organic Anion Transporters ; metabolism ; Prostaglandins ; analysis ; RNA, Messenger ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo identify associated proteins involved in the molecular response of ischemic preconditioning (IPC) against intestinal ischemia/reperfusion (II/R) in the intestinal mucosa of rats.

METHODSSixteen SD rats were randomly divided into II/R and IPC groups. II/R injury in rats was produced by clamping superior mesenteric artery for 60 min followed by 60 min reperfusion. IPC was elicited by 20 min ischemia and 5 min reperfusion before index ischemia. The intestinal mucosa was scratched immediately after 60 min of reperfusion and total proteins were separated by immobilized pH gradient (IPG) based on two-dimensional gel electrophoresis (2-DE). The differentially expressed proteins were analyzed using Image Master 2D Elite 5.0 image analysis software and identified by MALDI-TOF-MS. The biological information of these proteins was searched in the database of these peptide mass finger-printing (PMF). Western blotting and RT-PCR were used to validate the differentially expressed proteins.

RESULTSImage analysis revealed that averages of 1404+/-20 and 1338+/-20 were detected in II/R and IPC groups. A total of 10 spots yielded good spectra, and 8 spots matched with known proteins after database searching. These proteins were mainly involved in anti-oxidation, inhibiting apoptosis and energy metabolism. Western blot confirmed up-regulation of aldehyde dehydrogenase and RT-PCR confirmed up-regulation of aldose reductase in IPC group.

CONCLUSIONThe clues provided by comparative proteome strategy will shed light on molecular mechanisms of IPC against II/R injury.

Animals ; Intestinal Diseases ; metabolism ; pathology ; Intestinal Mucosa ; metabolism ; pathology ; Ischemic Preconditioning ; Male ; Proteomics ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology

OBJECTIVEIn this study, a growing rat model of zinc deficiency was established to investigate the effect of zinc deficiency on intestinal mucosal morphology and digestive enzyme activity as well as to provide a scientific basis for zinc supplementation therapy in patients with diarrhea.

METHODThree-week-old weaned Sprague-Dawley male rats (n = 30) were randomly divided into 3 groups with 10 in each: rats in the control group (ZA) were fed with a normal diet containing 30 µg/g zinc; rats in the zinc deficient group (ZD) were fed with a zinc-deficient diet containing 0.4 µg/g zinc (refer to AIN-76 formula); and rats in the paired fed group (PF) were fed with a normal diet, but the food intake was limited to intake of rats in ZD group in the previous day. All rats were provided with deionized water for drinking. Their body weight was measured and the food intake during the previous day was recorded early in the morning of the following day. Symptoms of zinc deficiency, such as anorexia, diarrhea, dermatitis, and growth retardation, were observed. Two weeks later, the rats were sacrificed and serum zinc concentration was measured. Jejunal mucosa was taken for biopsy and was stained with hematoxylin and eosin (HE). The height ratio of the jejunal mucosal villi and crypts was measured. In addition, the activity of lactase in the jejunal mucosal brush border, γ-glutamyl peptidase (GGT), and aminopeptidase N (APN) were measured.

RESULTThe average weight of the rats in the ZA, ZD, and PF groups at the beginning of the experiment was (67.4 ± 5.3) g, (64.7 ± 4.8) g, and (66.5 ± 4.1) g, respectively, and the average daily food intake was (11.2 ± 1.0) g, (11.6 ± 1.6) g, and (11.2 ± 1.4) g, respectively. The intergroup differences were not significant. On the 7(th) day of experiment, no significant differences in average food intake were observed between the ZD group and the ZA and PF groups, but the average body weight in the ZD group was significantly lower than that in the ZA and PF groups (P < 0.01). At the end of the experiment (2 weeks), the average weight in the ZD group (112.0 ± 11.5) g was significantly lower than that in the ZA (164.0 ± 15.9) g and PF groups (137.5 ± 16.2) g. The average food intake in the ZD group (13.4 ± 5.1) g was significantly lower than that in the ZA group (18.2 ± 2.4) g (P < 0.01). Serum zinc level in the ZD group (733 ± 231) µg/L was significantly lower than that in the ZA (1553 ± 159) µg/L and PF groups (1457 ± 216) µg/L (P < 0.01). The height ratio of jejunal mucosa villus and crypt in the ZA, ZD, and PF groups was 2.98 ± 0.5, 2.77 ± 0.5, and 2.81 ± 0.7, respectively, and lactase activity was (26.1 ± 15.0) U/mg, (27.4 ± 12.8) U/mg, and (40.8 ± 18.5) U/mg, respectively, without significant intergroup differences. The GGT activity in the jejunal mucosa in the ZD group (12.7 ± 6.5) U/g was significantly lower than that in the ZA (19.1 ± 10.4) U/g and PF groups (18.5 ± 7.7) U/g, but the difference was not significant. The activity of APN in the jejunal mucosa in the ZD group (25.5 ± 7.5) U/g was significantly lower than that in the ZA (48.7 ± 16.8) U/g and PF groups (43.9 ± 14.5) U/g (P < 0.01).

CONCLUSIONZinc deficiency can cause loss of appetite, weight loss, and decreased activity of peptidase in the jejunal mucosal brush border. Zinc deficiency has little effect on the height ratio of the villus and crypt and lactase activity, thereby indicating that zinc deficiency may first affect protein digestion and absorption.

Animals ; Intestinal Mucosa ; enzymology ; metabolism ; pathology ; Jejunum ; metabolism ; pathology ; Lactase ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Zinc ; deficiency

Enterocolitis, Necrotizing ; metabolism ; pathology ; Female ; Humans ; Immunohistochemistry ; Infant, Newborn ; Intestinal Mucosa ; metabolism ; pathology ; Male ; Platelet Activating Factor ; metabolism

The pathogenesis of inflammatory bowel disease (IBD) is not fully elucidated. However, it has been considered that inflammatory macrophages may be involved in the imbalance of the intestinal mucosal immunity to regulate several signaling pathways, leading to IBD progression. The ratio of M1 to M2 subtypes of activated macrophages tends to increase in the inflamed intestinal section. There are challenges in the diagnosis and treatment of IBD, such as unsatisfactory specificity of imaging findings, low drug accumulation in the intestinal lesions, unstable therapeutic efficacy, and drug-related systemic toxicity. Recently developed nanoparticles may provide a new approach for the diagnosis and treatment of IBD. Nanoparticles targeted to macrophages can be used as contrast agents to improve the imaging quality or used as a drug delivery vector to increase the therapeutic efficiency of IBD. This article reviews the research progress on macrophage-targeting nanoparticles for the diagnosis and treatment of IBD to provide a reference for further research and clinical application.
Humans ; Inflammatory Bowel Diseases/therapy* ; Intestines ; Macrophages/metabolism* ; Intestinal Mucosa/pathology* ; Nanoparticles

OBJECTIVETo explore the role of annexin A2 (ANXA2) expression in the intestinal mucosa in the pathogenesis of inflammatory bowel disease (IBD).

METHODSIntestinal or colonic mucosal biopsy samples were obtained from 54 patients with ulcerative colitis (UC), 37 with Crohn's disease (CD), and 15 healthy control subjects. Immunohistochemistry was employed to examine the expression of ANXA2 in the intestinal mucosa, and mRNA expression of ANXA2 was detected using real-time PCR.

RESULTSImmunohistochemistry showed a ANXA2 positivity rate of 83.3% (45/54) in patients with UC, 27.0% (10/37) in patients with CD, and 53.3% (8/15) in the control subjects. ANXA2 expression in the intestinal or colonic mucosa was significantly up-regulated in patients with UC compared with the patients with CD and healthy control subjects, but was significantly lower in patients with CD than in the healthy controls (P<0.05). The expression levels of ANXA2 were strongly associated with the severity of clinical manifestations and the histopathological grades of UC (P<0.05). Compared with the healthy controls and patients with CD, patients with UC showed a significantly increased ANXA2 mRNA expression level in the inflamed mucosa of UC (P<0.05).

CONCLUSIONANXA2 can serve as a marker for differential diagnosis of IBD, and its up-regulated expression is closely related to the pathogenesis of UC.

Annexin A2 ; metabolism ; Case-Control Studies ; Colitis, Ulcerative ; metabolism ; pathology ; Crohn Disease ; metabolism ; pathology ; Female ; Humans ; Inflammatory Bowel Diseases ; metabolism ; pathology ; Intestinal Mucosa ; metabolism ; pathology ; Male

OBJECTIVETo investigate the role of integrin α4β7 in the development of ulcerative colitis (UC) in rats.

METHODSSixty Sprague-Dawley rats were randomly divided into the control group (acetone enema), the model group (2,4-dinitrochlorobenzene, DNCB enema), and the α4 intervention group. Colonic mucosa of different groups was observed and compared in terms of pathology and cytokine changes(IL-2 and IL-6) using ELISA. Semi-quantitative RT-PCR was used to detect the colon α4β7 expression. Integrin α4β7(+) lymphocytes in the portal vein of rats were determined by flow cytometry.

RESULTSThe expression of α4 mRNA was 0.68±0.24 in the model group and 0.58±0.37 in the intervention group, and the expression of β7 mRNA was 0.84±0.37 in the model group and 0.65±0.30 in the intervention group, which were all significantly higher as compared to those in the control group(0.15±0.13 for α4 and 0.24±0.62 for β7, P<0.01). The proportions of integrin α4β7 positive lymphocytes in the portal vein in the model group and intervention group were significantly higher than that in the control group [(76.7±8.2)% and (68.2±7.6)% vs. (14.7±6.7)%, P<0.01]. The expression of IL-2 and IL-6 and the result of macroscopic and microscopic scores in the intervention group were lower than those in the model group(P<0.05).

CONCLUSIONSHigh expression of α4β7 may play an important role in experimental colon mucosa inflammation in rats with ulcerative colitis. The blockade of integrin α4β7 may be a potential target to reduce colonic mucosa inflammation.

Animals ; Colitis, Ulcerative ; metabolism ; pathology ; Colon ; metabolism ; pathology ; Disease Models, Animal ; Female ; Integrins ; metabolism ; physiology ; Interleukin-2 ; metabolism ; Interleukin-6 ; metabolism ; Intestinal Mucosa ; pathology ; Rats

OBJECTIVETo investigate the expression differences of apoptosis-inducing factor (AIF) and caspase-3 among colorectal carcinoma, adenoma and normal mucosa, and to identify the relationship between AIF and caspase-3 expression in colorectal adenoma-carcinoma sequence.

METHODSFormalin-fixed paraffin embedded colorectal tissues from 174 cases, including 84 adenomas, 72 carcinomas, and 18 normal mucosa, were examined for expression of AIF and caspase-3 by streptavidin-peroxidase (SP) immunohistochemistry.

RESULTSThe positive rates of AIF and caspase-3 in colorectal adenoma were higher than those in normal mucosa (P <0.05). The positive rate of AIF in adenoma showed no significant difference compared to colorectal carcinoma (P >0.05). However, caspase-3 expression in adenomas was significantly higher than that in carcinoma (P <0.05). The positive rate of AIF in tubular adenoma was significantly higher than that in villous adenoma (P <0.05), while the positive expression rate of caspase-3 in the two types of adenoma showed no significant difference (P >0.05). AIF expression had no prominent correlation with the caspase-3 expression (P >0.05).

CONCLUSIONSThe dysregulation of caspase-independent pathway of apoptosis may be an early event in the development of colorectal carcinogenesis, while the dysregulation of the caspase-dependent pathway of apoptosis may be one of contributing factors of colorectal carcinogenesis. The caspase-independent pathway of apoptosis and the caspase-dependent pathway of apoptosis are two relatively independent pathways in colorectal carcinogenesis.

Adenoma ; metabolism ; pathology ; Adult ; Aged ; Apoptosis Inducing Factor ; metabolism ; Caspase 3 ; metabolism ; Colorectal Neoplasms ; metabolism ; pathology ; Female ; Humans ; Intestinal Mucosa ; metabolism ; pathology ; Middle Aged ; Young Adult