The effect of nitrogen mustard intoxication on glucose absorption from the small intestine of the rat

Methyl bis (β-chlorethyl) amine (HN₂) was administered as a single intraperitoneal dose to male Sprague-Dawley rats. Animals were given either a median lethal dose and perfused one day after treatment or were given a larger dose and perfused two days after treatment. Intestinal segments were perfused in vivo and samples of effluent were collected and measured for glucose using the glucose oxidase method.

Animals treated with the larger dose of HN₂ displayed significant reduction in intestinal dry weight. The average water content of intestinal segments derived from treated animals did not differ significantly from that in controls.

Steady-state glucose absorption, obtained from data collected during the last 40 minutes of the perfusion period, was found to be significantly reduced in animals treated with drugs when intestinal absorption for control and treated animals was adjusted for water movement but not for dry intestinal weight and length. However, when glucose absorption was adjusted for dry tissue mass and length as well as for water movement, no significant differences in intestinal glucose absorption between control and treated rats were observed. Alterations can therefore be attributed to loss of intestinal tissue rather than to loss in the ability of the intestinal mass to absorb glucose.

     

Structural and Morphometric Analysis of Murine Small Intestine after Indomethacin Administration

Ettarh RR, Carr KE. Structural and morphometric analysis of murine small intestine after indomethacin administration. Scand J Gastroenterol 1993;28:795-802.

Indomethacin, a nonsteroidal anti-inflammatory drug, induces the formation of gastrointestinal ulceration both in experimental animals and in humans. A study of indomethacin-induced ulcers in the mouse showed that two doses of indomethacin, each administered subcutaneously at 85 mg/kg body weight, induced well-defined gastrointestinal ulcers in C57 mice, accompanied by inflammatory and vascular changes in the stomach and small intestine. Maximal damage was observed 20 h after the second dose of indomethacin. Morphometric analysis identified changes in all compartments of the small intestine. There was a marked reduction in the length of the small intestine, intestinal dilatation, a significant decrease in villous height, with the formation of subepithelial blisters or blebs within villi, and submucosal vascular dilatation. There was no change in the number of villi or of submucosal arterioles or in the total amount of muscle present in the wall of the intestine. The tissue changes identified in this study may have implications for gut function at specific periods during indomethacin treatment.     

Induction and maintenance of mucosal enterokinase activity in proximal small intestine by a genetically determined response to mediated sodium transport

Mucosal enterokinase activity was established at intervals throughout the small intestine in guinea-pigs; maximum activity was present in the duodenum and proximal jejunum in new born as well as adult animals. Transposition of 5 cm lengths of small gut from the high enterokinase containing proximal region to the distal intestine and vice versa showed that mucosal enterokinase activity in the transposed segments was little changed after several weeks of healthy life. Isolation of proximal jejunal loops from luminal continuity resulted in the fall of mucosal enterokinase activity to minimal levels within 16 hours. Low levels of mucosal enterokinase activity were identified in loops of both proximal and distal jejunum 12 weeks after isolation. Luminal perfusion studies in vivo in proximal jejunal loops 24 hours after isolation showed that mucosal enterokinase activity could be restored to near normal levels within four to six hours by luminal sodium in the presence of active pancreatic endopeptidases, oligopeptides, L-amino acids, or D-glucose but not D-amino acids or D-fructose. Near normal mucosal enterokinase activity persisted in the loops for as long as luminal perfusion with 144 mM sodium and L-lysine or trypsin was maintained (24 hours). The time course of the restoration of mucosal enterokinase activity was compatible with an initial precursor activation as well as biosynthesis. The requirement for luminal sodium appeared to be absolute regardless of the co-substrate and supports the conclusion that mucosal enterokinase activity is dependent on mediated sodium transport. The ability of proximal intestinal enterocytes to respond to sodium flux with an increase in enterokinase activity is a property determined in intrauterine life: distal intestinal enterocytes may have functioning structural genes for enterokinase but appear to be unable to respond.     

Putrescine as a source of instant energy in the small intestine of the rat

Background and aims—It has been suggested thatputrescine acts as a growth factor in the gut, but its exact functionin some aspects of cellular metabolism is still in question. The aim of the present work was to identify some functions of putrescine in smallbowel metabolism.
Animals—Rats (about 80 g), in groups of five, weregiven either phytohaemagglutinin- or lactalbumin-containing diets,fed ad libitum or were fasted for 48 hours and re-fed for six or twelve hours before being killed.
Methods—Uptake of intraperitoneally orintragastrically administered [¹⁴C]putrescine and itsconversion to succinate by the rat small bowel mucosa was measured.Tissue polyamine and succinate contents were measured by highperformance liquid chromatography and amino acid analysis respectively.
Results—Uptake of putrescine by the small bowelmucosa from the systemic circulation and conversion of about 30% ofthis to succinate occurs in the epithelium of the healthy small bowel. Compared with rats given food ad libitum, putrescine uptake was doubledin fasted animals and more than 70% of it was converted to succinate.All these changes returned to control values on refeeding. Using phyto-haemagglutinin induced gut growth as a model, the uptake ofputrescine from the systemic circulation by the serosal side of thesmall intestinal epithelium was increased immediately after growth wasstimulated. During phytohaemagglutinin induced growth of the gut,putrescine was converted to succinate in the same proportion as inthe healthy small bowel.
Conclusions—The experiments identified a novelfunction for putrescine in gut metabolism: it can be used as an instantenergy source when required.

Keywords:putrescine; luminal uptake; phytohaemagglutinin; succinate; basolateral uptake; small bowel

     

The Relationship between Body Iron Stores and Ferritin Turnover in Rat Liver and Intestinal Mucosa

A single dose of oral or parenteral iron is known to stimulate ferritin synthesis in the liver and small intestine in experimental animals. A study has been carried out on the ferritin content and ferritin turnover in rat liver and intestinal mucosa in iron deficient, normal and iron loaded animals. [I-¹⁴C]DL-leucine incorporation into ferritin was used as a measure of its synthesis.
A significantly greater ferritin accumulation was found in the intestinal mucosa of the group of iron loaded animals compared with normal or iron deficient rats ( P < 0.001). In the liver the ferritin protein, ferritin iron and labelled ferritin content was significantly different between all three groups ( P < 0.001), the amounts being higher in the iron loaded animals and lower in the iron deficient animals when compared with the normal group. These results may explain how the absorption of iron in the small intestine is controlled by body iron stores.     

康尔胃2号药效学研究

目的:观察康尔胃2号对动物胃肠运动及胃粘膜损伤的影响.方法:将5种动物模型分为空白对照组、阳性药物对照组及康尔胃2号大、中、小剂量组进行干预,比较各组作用及疗效.结果:康尔胃2号能防治乙醇致大鼠胃粘膜损伤,促进正常小鼠胃排空和小肠推进,对大鼠体内胃自发活动有抑制作用,对体外兔肠自发活动及氯化钡负荷下肠自发活动有抑制作用.结论:康尔胃2号有调整动物胃肠运动,保护胃粘膜等药理作用.     

Lipids infused into the jejunum accelerate small intestinal transit but delay ileocolonic transit of solids and liquids

Background—Various nutrients areknown to alter small intestinal motility patterns although their effecton transit of fluids and solids in man is not clear.
Aims—To determine small intestinaltransit of solids and liquids during perfusion with lipids, protein,and non-energy solutions.
Methods—Twenty eight healthyvolunteers received a jejunal infusion (1 ml/ minute for 30 minutes) ofone of four solutions: a lipid or a protein solution (4.18 J/ml), anon-absorbable electrolyte solution containing polyethylene glycol, or0.9% sodium chloride. As solid phase marker 1 g of amberlite resinpellets labelled with ¹¹¹InCl₃ was added;^99mTc DTPA was used as a fluid phase marker. Images wereobtained on a gamma camera at 10 minute intervals for four hours oruntil all radiolabel was detected in the colon.
Results—Intestinal transit ofsolids and liquids from the duodenojejunal junction to the caecum wassimultaneous, and independent of the energy content of the solutioninfused. Lipid infusion accelerated transit through the small intestinebut delayed transport of chyme along the ileocolonic junction. Afterprotein small intestinal transit was slowest; ileocolonic transit onthe other hand was fastest with protein. Transit of the non-energysolutions was in between that of the nutrient solutions.
Conclusions—Transit times throughthe small intestine and the ileocolonic junction were influenced by theluminal contents. In the small intestine fat induced significantlyfaster transit compared with proteins, but delayed ileocolonic transit.Once in the small intestine, solids and liquids transit the small bowel together, independent of the luminal content.

Keywords:small intestine; ileocolonic junction; transit; nutrients; lipids; proteins

     

Small intestinal absorption of polyethylene glycol 400 to 1,000 in the portacaval shunted rat

Functional changes of the intestinal barrier that may occur after the creation of a portacaval shunt (PCS) were investigated. After chronic PCS in the rat, the intestinal absorption of and the jejunal permeability to the inert polymer marker polyethylene glycol (PEG) with molecular weight (Mw) ranging from 400 to 1,000 g/mol were investigated. The PEG mixture was orally fed to PCS and sham-operated rats, and urine was collected for 24 hours to obtain the urinary recovery of the different PEG polymers as a measure of intestinal absorption. To study the intestinal permeability, segments from the proximal small intestine were incubated in diffusion chambers with the PEG mixture on the mucosal side, and samples were withdrawn from the serosal side for analysis. The urinary recovery for the PEGs increased (P < .01) while the tissue permeability decreased (P < .001) in the PCS group rats in comparison with Sham-operated rats. The increased absorption in vivo was caused neither by altered renal clearance, nor by changed portal blood pressure. The decreased jejunal permeability in the PCS rats could be explained by a reduction of the mucosal area by shortening of the microvilli. This discrepancy indicates that changes in permeability and absorption may not be parallel during PCS. It is possible that these changes also may be affected by nutritional factors, drug therapy, as well as toxic substances.     

Dietary fibre and intestinal microflora: effects on intestinal morphometry and crypt branching

^a Anatomy Department, Medical Biology Centre, Queen's University of Belfast, ^b Robert Gordon University, Kepplestone, Aberdeen, ^c Imperial Cancer Research Fund, Histopathology Unit, Lincoln's Inn Fields, London

Correspondence to: Dr R A Goodlad, Imperial Cancer Research Fund, 35-43 Lincoln's Inn Fields, London WC2A 3PN, UK.

Accepted for publication 19 January 1998

Background—Fermentable dietary fibre has many effects on the gastrointestinal tract. One is to alter epithelial crypt cell proliferation, especially in the colon. A discrepancy between epithelial cell production rates and intestinal weights has been noted previously: crypt cell production rates only increase if bacterial fermentation occurs, but intestinal wet weight can increase in the same animals without bacterial fermentation of fibre.
Aims—To quantify intestinal cell populations in order to resolve the above paradox.
Methods—Conventional and germ-free rats were fed fibre-free or fibre supplemented diets and their intestines were quantified by morphometry.
Results—There was evidence of fibre associated muscle hypertrophy in the colon, but the main effect of fibre was an increase in the number of crypts per circumference and also the number of branched crypts in the proximal colon in both groups. There was also a large increase in the number of branched crypts in the mid colon of the germ-free rats (both fibre-free and fibre supplemented). Fibre had a direct (bacteria independent) effect on goblet cells in the small intestine and a direct effect on the goblet cells in the colon, which was attenuated by the presence of bacteria. There was a notable decline in the number of enteroendocrine cells in the small intestine of the germ-free animals.
Conclusions—Fibre has several direct and indirect effects on the gut. In the proximal colon it can directly increase the number of crypts present. This provides a means for increasing intestinal mass in addition to intestinal crypt cell production.
(GUT 1998;:799-806)

Keywords: fibre;  fermentation;  microflora;  mucus;  intestine;  epithelium

     

A morphological and histochemical study of the large intestine of white mice with experimental trichocephaliasis and after the action of some anthelmintic preparations]

Administration of levamisole, oxphendasole in dose 10 mg/kg and especially of ivomeck in dose 0.01 ml/kg of body weight damages the large intestine mucosa of intact mice and of mice with experimental T. muris infection. Epithelial cells dystrophy, the goblet cells destruction and the diffuse leucocytes infiltration of the intestinal wall, maximal 12 hours after the drugs administration, were most marked in animals treated with ivomeck. Pathomorphological changes in the gut mucosa after the drug administration to infected animals were significantly higher than in intact ones. That permits to conclude that the damage of the intestinal wall is due to the toxicity of the drugs, and perhaps with the damage of mucosa by the nonspecific (allergic) response to the chemotherapy.     

The role of xanthine oxidase in platelet activating factor induced intestinal injury in the rat

Background—Xanthine oxidase (XO) isan important source of reactive oxygen species in the small intestine.
Aims—To examine the interaction ofplatelet activating factor (PAF), XO, and neutrophils in mediatingintestinal injury in rats.
Methods—Two doses of PAF were usedto induce either reversible hypotension, or irreversible shock withintestinal necrosis. The activities of XO, and its precursor xanthinedehydrogenase (XD), in both the whole intestinal tissue and epithelialcells, were measured. XO was localised by histochemical staining.
Results—PAF dose dependentlyinduced an increase in XO activity, predominantly in the ilealepithelium, without altering the total activity of XD+XO. Most of theXD to XO conversion was via proteolysis. PAF induced XO activation andintestinal injury were prevented by prior neutrophil depletion. PAFinduced XO activation is probably not due to reperfusion, as XOactivation preceded the recovery of mesenteric flow. Allopurinolpretreatment substantially inhibited intestinal neutrophilsequestration induced by high dose (but not low dose) PAF.
Conclusions—PAF rapidly activatesintestinal XO through proteolytic XD-XO conversion, predominantly inthe ileal epithelium. This effect is mediated by neutrophils. XOactivation promotes PAF induced polymorphonuclear leucocytesequestration in the intestine.

Keywords:xanthine dehydrogenase; reactive oxygen species; leucocyte adhesion; neutrophils; shock

     

Mucin gene expression in human embryonic and fetal intestine

Background—The intestinal epithelium is coveredby a continuous layer of mucus which is secreted by well differentiatedepithelial cells. Disregulation of the expression of mucins has beenreported to have possible implications in the neoplastic process which affects intestinal mucosae. It is well known that preneoplastic andneoplastic tissues can express fetal phenotypic characteristics.
Aims—To assess whether the expression of mucingenes in the intestinal tract is linked to the stage of cellulardifferentiation and tissue development, by studying the expression ofsix mucin genes in human fetal small intestine and colon, and alsoadult tissues.
Methods—In situ hybridisation was used to studymRNA expression of MUC2, MUC3, MUC4, MUC5B, MUC5AC, and MUC6 in 32 human embryos and fetuses (6.5-27 weeks gestation). Normal adultmucosae were used as controls.
Results—Three mucin genes, MUC2, MUC4, andMUC5AC, were differently expressed in fetal intestine compared withexpression in normal adults.
Conclusion—These differences in mucin geneexpression suggest a possible regulatory role for these products inintestinal epithelial cell differentiation.

Keywords:mucin genes; mucins; intestine; differentiation; human fetus

     

The influence of aging on intestinal absorption of vitamin B12 and niacin in rats

The intestinal absorption of doses of vitamin B₁₂ and of niacin was examined in 6, 12, and 24 months old female Wistar rats. Rats were dosed via stomach tube with radioactive forms of the vitamins and were killed 16 hours later. Percent of the dose remaining in the stomach and gastro intestinal tract andthe collected feces was determined. Absorption of the two vitamins was not influenced by the age of the animals.     

Drug enterocyte adducts: possible causal factor for diclofenac enteropathy in rats

BACKGROUND & AIMS: Enteropathy is a frequent complication of diclofenac and other nonsteroidal anti-inflammatory drugs, yet little is known about the underlying mechanism. One possibility is that reactive metabolites of diclofenac form adducts with enterocyte macromolecules, as previously shown for liver. We addressed this possibility by using immunohistochemistry to detect diclofenac adducts. METHODS: Rats were treated orally with diclofenac (10-100 mg/kg) and killed after 1-24 hours, and their gastrointestinal (GI) tracts were evaluated for ulcer number and area. Adduct distribution and intensity were assessed by immunohistochemistry by using a technique to simultaneously process and stain multiple intestinal rings. RESULTS: Drug treatment led to dose-dependent formation of both adducts and ulcers only in small intestine and only in animals with intact enterohepatic circulation. Adducts formed within enterocytes by 1 hour, translocated to the brush border, preceded ulceration and vascular protein leakage, and were intense at sites of ulceration. Adducts and ulcers exhibited a parallel distribution within intestinal quintiles: 3rd > 5th > 1st. CONCLUSIONS: Diclofenac treatment resulted in the formation of drug adducts in enterocytes. Because this molecular change occurred before ulceration, was dose dependent, and exhibited concordant distribution with extent of ulceration, the results suggest a causal role for drug adduct formation in diclofenac enteropathy.     

Activation of phosphorylating-p38 mitogen-activated protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury

AIM: To investigate the expression of phosphorylating p38 mitogen-activated protein kinase (MAPK) in rat small intestine after ischemia-reperfusion (I/R) insult and its relationship with the localization of intestinal stem cells. METHODS: Forty-eight Wistar rats were divided randomly into three groups, namely intestinal ischemia-reperfusion group (R), intestinal ischemia group (I) and sham-operated control group (C). In group I, the animals were killed 45 minutes after superior mesenteric artery (SMA) occlusion, while in group R the rats sustained SMA occlusion for 45 minutes and reperfusion for 2, 6, 12 or 24 hours respectively. In sham-operated control group, SMA was separated, but without occlusion. The activity of plasma diamine oxidase (DAO) was determined. Intestinal tissue samples were also taken for histological analysis and immunohistochemical analysis of MAPK p38 detection and intestinal stem cell localization. RESULTS: The changes in histological structure and plasma DAO levels indicated that the intestinal barrier was damaged after intestinal I/R injury. In group C and I, each crypt contained 5-6 p38 MAPK positive cells, which were mainly located in the lower region of the crypts. This was consistent with the distribution of intestinal stem cells. The presence of positive cells in crypts increased with the time of reperfusion and reached its peak at 12 hours after reperfusion (35.6 %). CONCLUSION: After intestinal I/R injury, the expression of phosphorylating-p38 MAPK in small intestine increased with the duration of reperfusion, and its distribution coincided with that of intestinal stem cells and their daughter cells, indicating that phosphorylating-p38 might be a possible marker of intestinal stem cells.     

Preclinical Efficacy of Melatonin to Reduce Methotrexate-Induced Oxidative Stress and Small Intestinal Damage in Rats

Background

Methotrexate is widely used as a chemotherapeutic agent for leukemia and other malignancies. The efficacy of this drug is often limited by mucositis and intestinal injury, which are the major causes of morbidity in children and adults.

Aim

The present study investigates whether melatonin, a powerful antioxidant, could have a protective effect.

Method

Rats were pretreated with melatonin (20 and 40 mg/kg body weight) daily 1 h before methotrexate (7 mg/kg body weight) administration for three consecutive days. After the final dose of methotrexate, the rats were sacrificed and the small intestine was used for light microscopy and biochemical assays. Intestinal homogenates were used for assay of oxidative stress parameters malondialdehyde and protein carbonyl content, and myeloperoxidase activity, a marker of neutrophil infiltration as well as for the activities of the antioxidant enzymes.

Result

Pretreatment with melatonin had a dose-dependent protective effect on methotrexate (MTX)-induced alterations in small intestinal morphology. Morphology was saved to some extent with 20 mg melatonin pretreatment and near normal morphology was achieved with 40 mg melatonin pretreatment. Biochemically, pretreatment with melatonin significantly attenuated MTX-induced oxidative stress (P < 0.01 for MDA, P < 0.001 for protein carbonyl content) and restored the activities of the antioxidant enzymes (glutathione reductase P < 0.05, superoxide dismutase P < 0.01).

Conclusion

The results of the present study demonstrate that supplementation by exogenous melatonin significantly reduces MTX-induced small intestinal damage, indicating that it may be beneficial in ameliorating MTX-induced enteritis in humans.     

Insulin-producing cells in the gut of freshwater bivalve molluscs Anodonta cygnea and Unio pictorum and the role of insulin in the regulation of their carbohydrate metabolism

In the epithelium of the small intestine of freshwater bivalve molluscs Anodonta cygnea and Unio pictorum cells were found which are reactive with antibodies to mammalian insulin. The apical parts of the cells are extended to the intestinal lumen. The nuclei are located in the basal parts resting on the basement membrane. The cytoplasm contains fine aldehyde fuchsin (AF)-positive and periodic acid-Schiff (PAS)-positive granules. The height of the immunostained cells is 10 to 15 times their width. Glucose, insulin, and anti-insulin serum (AIS) were injected into the molluscs and the changes in glycaemia, muscle glycogen content, and muscle glycogen synthetase activity induced by these substances were observed. Immunoreactive insulin (IRI) content in haemolymph and in gut extracts was assayed in experiments on the same animals; the quantity of AF-positive cells was calculated in the region of the gut where immunostained cells were present. The action of insulin on glucose uptake by slices of mollusc muscles was also studied. The results of the experiments demonstrate that insulin or some substance closely related to insulin is actually produced in the small intestine of the molluscs studied and makes a direct contribution to the regulation of carbohydrate metabolism in these animals.     

The effect of alpha-glucosidase inhibition on intestinal disaccharidase activity in normal and diabetic mice

Acarbose is a potent alpha-glycosidase inhibitor which decreases postprandial hyperglycemia when administered with a carbohydrate-containing meal. The genetically diabetic mouse C57 BLKsJ db/db represents a model of type II, noninsulin dependent diabetes mellitus. Characteristic features of this animal include hyperglycemia, hyperinsulinemia, hyperphagia, and the development of obesity and widespread pathologic abnormalities. To evaluate the effects of Acarbose on intestinal disaccharidase activity, groups of normal and diabetic mice were given Acarbose as a drug-food mixture in doses of 20 (A-20) and $\text{40 (A-40) mg}\text{100 g}$ food. Sucrase activity was measured in intestinal homogenates and on the mucosal surface of proximal, middle, and distal segments of jejunoileum. In normal mice, sucrase activity was significantly increased in mid- and distal-intestinal segments following 2 wk of Acarbose in both A-20 and A-40 groups. No changes were noted following 5 and 10 days of drug treatment. Acarbose did not influence body weight, food:water intake or fasting blood glucose. When compared to normal mice, untreated diabetics had significantly more protein, DNA, and sucrase activity throughout the small intestine. Following 10 wk of Acarbose administration, both A-20 and A-40 groups showed increased sucrase activity in intestinal homogenates of distal segments. Surface mucosal sucrase activity however was slightly decreased in proximal intestinal segments as a result of drug therapy, with no changes in middle and distal segments. Acarbose did not influence body weight, food intake or fasting blood glucose, but water consumption and glucosuria were significantly decreased. Experimental diabetes mellitus is associated with significant alterations in enzyme activity and protein content of the brush border membrane of the small intestine. Acarbose administration influences both sucrase activity and distribution in normal and diabetic mice. The mechanisms responsible for these changes and their potential clinical importance remain to be determined.     

Protection effect of Emodin pretreatment on intestinal I-RI damage of intestinal mucosa in ratsa

Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P0.05),SOD level was significantly higher than that of model group(P0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.     

Insulin-like growth factor-I stimulates Na+-dependent glutamine absorption in piglet enterocytes

Agents that enhance intestinal glutamine transport may be useful under conditions in which intestinal mucosal function is compromised. Here we examined whether oral administration of insulin-like growth factor (IGF-I) stimulates absorption of l-glutamine in piglet intestine. Colostrum-deprived piglets received human recombinant IGF-I (3.5 mg/kg/day) or vehicle orogastrically every 8 hr for four days after birth. Piglets were killed on day 5 and the proximal jejunum was removed. Basal electrical parameters and l-glutamine-stimulated changes in short-circuit current were measured in muscle-stripped tissues, and rates of l-glutamine uptake were measured in everted jejunal sleeves. Oral IGF-I had no effect on jejunal mucosal mass. Short-circuit current responses to mucosal addition of 10 mM l-glutamine were increased by oral IGF-I. Total and carrier-mediated uptakes of l-glutamine per milligram were greater in tissues from IGF-I-treated piglets due to a significantly greater maximal rate of uptake (J _max). Thus, oral administration of IGF-I stimulates Na⁺-dependent glutamine absorption in piglet small intestine, an effect that is independent of changes in intestinal mucosal mass.