Rat Small Intestinal Mucosa Research Articles

ANTIULCER ACTIVITY OF PLACENTAL CRYOEXTRACT IN EXPERIMENTAL INDOMETHACIN-INDUCED ULCEROGENESIS

Aim. The side effects associated with the use of indometacin are noted by about 30-60% of patients, therefore, in this context the problem of adverse event rate reduction is still relevant today. Cryopreserved placental extract (CEP) attracted our attention as a means of pathogenetic correction of the ulcerogenic action of indomethacin. The aim of the paper is to characterize the antiulcer activity of cryopreserved placenta extract on a model of indomethacin-induced ulcerogenesis.
 Materials and Methods. In vivo experimental studies were performed on 28 nonlinear laboratory male rats weighing 200-220 g. Acute indomethacin-induced gastrointestinal injury was replicated by a single injection of indomethacin at 60 mg/kg in rats. Euthanasia of animals was performed after 4 hours after indomethacin administration.
 Results and Discussion. Macroscopic evaluation of the condition of the gastric mucosa showed that all animals had numerous pinpoint hemorrhages, and 49.2% of rats had mild hyperemia and abnormal folding. Evaluation of the condition of the small intestinal mucosa showed that 57.1% of rats injected with indomethacin alone had 11.1±4.1 ulcers per 10 cm of mucosa length. Prophylactic administration of esomeprazole led to a statistically significant (p<0.05) attenuation of the ulcerogenic effect of indomethacin on the gastric mucosa - the mean score of the mucosa was 3.9 times lower than in control rats and was 0.9±0.26.
 Conclusions. The combined use of indomethacin and CEP was associated with a 1.9-fold lower ulcer index as compared with rats administered indomethacin only, thus demonstrating the gastroprotective activity of CEP. In contrast to esomeprazole, the introduction of CEP has a pronounced enteroprotective effect, as indicated by the absence of damage to small intestinal mucosa in rats treated with the studied cryoextract and indomethacin.

Role of TLR4/NF-κB pathway in the damage of acute hypobaric hypoxia to small intestinal mucosa in rats.

The purpose of this study was to investigate the effect of acute hypobaric hypoxia (HH) exposure on small intestinal mucosa in rats and its underling mechanism. The pathological changes of rat small intestine mucosa were detected by HE staining. The expressions of TLR4 and NF-κB in the small intestine were detected by immunohistochemistry (IHC). The levels of Zonulin, TNF-α, IL-1β, and IL-6 in the serum were detected by ELISA. The proportion of natural killer (NK) cells and dendritic cell population in the small intestine was analyzed by flow cytometry. The mRNA and protein levels of TLR4, NF-κB, occludin, HIF-1α, and iNOS were detected by RT-qPCR and Western blot, respectively. Compared with the Control group, the HH groups had different degrees of injury in intestinal mucosa. Meanwhile, in the HH groups, it was also found the increased levels of Zonulin, TNF-α, IL-1β and IL-6 in the serum, the increased CD4+/CD8+T cells ratio and small intestine NK cells population, the increased mRNA and protein expression levels of small intestine TLR4, NF-κB, HIF-1α and iNOS, and the decreased mRNA and protein expression levels of occludin. Acute HH may damage the intestinal mucosa of rats by inducing TLR4/NF-κB pathway overexpression.

IIAEK Targets Intestinal Alkaline Phosphatase (IAP) to Improve Cholesterol Metabolism with a Specific Activation of IAP and Downregulation of ABCA1.

IIAEK (Ile-Ile-Ala-Glu-Lys, lactostatin) is a novel cholesterol-lowering pentapeptide derived from bovine milk β-lactoglobulin. However, the molecular mechanisms underlying the IIAEK-mediated suppression of intestinal cholesterol absorption are unknown. Therefore, we evaluated the effects of IIAEK on intestinal cholesterol metabolism in a human intestinal model using Caco-2 cells. We found that IIAEK significantly reduced the expression of intestinal cholesterol metabolism-associated genes, particularly that of the ATP-binding cassette transporter A1 (ABCA1). Subsequently, we chemically synthesized a novel molecular probe, IIXEK, which can visualize a complex of target proteins interacting with photoaffinity-labeled IIAEK by fluorescent substances. Through photoaffinity labeling and MS analysis with IIXEK for the rat small intestinal mucosa and intestinal lipid raft fractions of Caco-2 cells, we identified intestinal alkaline phosphatase (IAP) as a specific molecule interacting with IIAEK and discovered the common IIAEK-binding amino acid sequence, GFYLFVEGGR. IIAEK significantly increased IAP mRNA and protein levels while decreasing ABCA1 mRNA and protein levels in Caco-2 cells. In conclusion, we found that IIAEK targets IAP to improve cholesterol metabolism via a novel signaling pathway involving the specific activation of IAP and downregulation of intestinal ABCA1.

Injury of small intestinal mucosa in rats induced by aspirin and clopidogrel and the protective effect of teprenone

The purpose of this study was to investigate the injury of aspirin and clopidogrel on small intestinal mucosa in rats and the protective effect of teprenone. The study found that aspirin and clopidogrel could cause intestinal mucosal injury in rats, which was even worse with dual drugs. The mechanism of mucosal injury included free radical injury induced by aspirin and decreased synthesis of vascular endothelial growth factor (VEGF) by clopidogrel. Teprenone may repair intestinal mucosa via boosting VEGF level.

Effect of Omeprazole on Intestinal Mucosal Barrier After Hemorrhagic Shock in Rats

Objective: The aim of this study was to explain the effect of omeprazole on intestinal mucosal barrier after hemorrhagic shock in rats. Materials and methods: 81 rats were allocated to control, hemorrhagic shock model group and omeprazole group according to random number table, and each group was divided into three subgroups according to the time point of 0, 6, 12 h after HS and resuscitation. The rat model of hemorrhagic shock was induced by using the improved Wiggers method. Model group and omeprazole group were given physiological saline or omeprazole 30 mg/kg retention enema after the post-resuscitation. At three time points, the level of intestinal fatty acid binding protein (IFABP) in the serum was test by ELISA method, and the levels of serum endotoxin (LPS) was detected by dynamic turbidimetric method. The morphological changes of small intestinal mucosa in rats was observed under light microscope, VASP and ZO-1 mRNA expression was measured by RT-qPCR, while p-VASP and ZO-1 protein expression was measured by immunohistochemical method. Results: Compared with model group, serum endotoxin (LPS), fatty acid binding protein (IFABP) content gradually increased (P < 0.05, respectively), and intestinal mucosa damage was aggravate, VASP and ZO-1 gene expression were significantly down-regulation (P < 0.05, respectively) and p-VASP and ZO-1 protein expression were significantly depressed (P < 0.05, respectively). Conclusion: Omeprazole can significantly aggravate the intestinal mucosal barrier function by regulating VAASP and ZO-1 expression after hemorrhagic shock and resuscitation.

ラット小腸粘膜および組換えマウス型のβ-カロテン15,15’-モノオキシゲナーゼ活性に及ぼすリノール酸の影響

ラット小腸粘膜および組換えマウス型のβ-カロテン15,15’-モノオキシゲナーゼ活性に及ぼすリノール酸の影響

A novel class of α-glucosidase and HMG-CoA reductase inhibitors from Ganoderma leucocontextum and the anti-diabetic properties of ganomycin I in KK-Ay mice

Three new meroterpenoids, ganoleucin A-C (1–3), together with five known meroterpenoids (4–8), were isolated from the fruiting bodies of Ganoderma leucocontextum. The structures of the new compounds were elucidated by extensive spectroscopic analysis, circular dichroism (CD) spectroscopy, and chemical transformation. The inhibitory effects of 1–8 on HMG-CoA reductase and α-glucosidase were tested in vitro. Ganomycin I (4), 5, and 8 showed stronger inhibitory activity against HMG-CoA reductase than the positive control atorvastatin. Compounds 1, and 3–8 presented potent noncompetitive inhibitory activity against α-glucosidase from both yeast and rat small intestinal mucosa. Ganomycin I (4), the most potent inhibitor against both α-glucosidase and HMG-CoA reductase, was synthesized and evaluated for its in vivo bioactivity. Pharmacological results showed that ganomycin I (4) exerted potent and efficacious hypoglycemic, hypolipidemic, and insulin-sensitizing effects in KK-Ay mice.

The LKEKK synthetic peptide as a ligand of rat intestinal epithelial cell membranes

A tritium-labeled synthetic LKEKK pentapeptide corresponding to the sequences 16–20 of human thymosin-α1 and 131–135 of human interferon-α2 was obtained with a specific activity of 28 Ci/mmol. [3H]LKEKK was found to bind with high affinity (K d 3.7 ± 0.3 nM) to the membranes isolated from epithelial cells of rat small intestinal mucosa. The trypsin treatment of the membranes did not affect the binding, thus supporting the nonprotein nature of the peptide receptor. The binding of the labeled peptide was inhibited by unlabeled thymosin-α1, interferon-α2, and cholera toxin B subunit (K i 4.2 ± 0.4, 3.5 ± 0.3, and 4.7 ± 0.3 nM respectively). The pentapeptide did not affect the adenylate cyclase activity within the concentration range of 1–1000 nM.

Effects of ε-viniferin, a dehydrodimer of resveratrol, on transepithelial active ion transport and ion permeability in the rat small and large intestinal mucosa.

ε‐Viniferin is a dehydrodimer of resveratrol, a polyphenol synthesized in many plants, including grapevine. The present study investigated the effects of ε‐viniferin and resveratrol on epithelial secretory and barrier functions in isolated rat small and large intestinal mucosa. Mucosa–submucosa tissue preparations of various segments of the rat large and small intestines were mounted on Ussing chambers, and short‐circuit current (I sc) and tissue conductance (G t) were continuously measured. The mucosal addition of ε‐viniferin (>10−5 mol/L) and resveratrol (>10−4 mol/L) to the cecal mucosa, which was the most sensitive region, induced an increase in I sc and a rapid phase decrease (P‐1) followed by rapid (P‐2) and broad (P‐3) peak increases in G t in concentration‐dependent manners. Mucosal ε‐viniferin (10−4 mol/L), but not resveratrol (10−4 mol/L), increased the permeability of FITC‐conjugated dextran (4 kDa). The mucosal ε‐viniferin–evoked changes in I sc (Cl− secretion), but not in G t, were attenuated by a selective cyclooxygenase (COX)‐1 inhibitor and a selective EP 4 prostaglandin receptor. The mucosal ε‐viniferin–evoked increase in I sc was partially attenuated, and P‐2, but not P‐1 or P‐3, change in G t was abolished by a transient receptor potential cation channel, subfamily A, member 1 (TRPA1) inhibitor. Moreover, the mucosal ε‐viniferin concentration‐dependently attenuated the mucosal propionate (1 mmol/L)‐evoked increases in I sc and G t. Immunohistochemical studies revealed COX‐1–immunoreactive epithelial cells in the cecal crypt. The present study showed that mucosal ε‐viniferin modulated transepithelial ion transport and permeability, possibly by activating sensory epithelial cells expressing COX‐1 and TRPA1. Moreover, mucosal ε‐viniferin decreased mucosal sensitivity to other luminal molecules such as short‐chain fatty acids. In conclusion, these results suggest that ε‐viniferin modifies intestinal mucosal transport and barrier functions.

Detection of Gold Nanoparticles in Rat Organs by Transmission Electron Microscopy.

The effects of water-dispersed gold nanoparticles (8.0±0.9 nm in diameter) on the rat small intestinal mucosa and Peyer plaques, liver, and spleen were studied by electron microscopy. Water-dispersed gold nanoparticles injected into isolated intestinal loop not only accumulated in the small intestinal mucosa and Peyer plaques, but also penetrated into other organs, e.g. liver and spleen. Ultrastructural changes in the cells (hyperplasia of endoplasmic reticulum) were detected in the studied organs.

Methotrexate administration induces differential and selective protein tyrosine nitration and cysteine nitrosylation in the subcellular organelles of the small intestinal mucosa of rats

Gastrointestinal toxicity is one of the most frequent dose limiting side effects of methotrexate (MTX), a commonly used chemotherapeutic drug. Peroxynitrite (PON) overproduction is reported to contribute to MTX induced gastrointestinal mucositis. However, the consequence of PON overproduction i.e. protein tyrosine nitration and protein cysteine nitrosylation, the subcellular distribution of these modified proteins and their molecular weights have not been investigated yet. Mucositis was induced in Wistar rats by the administration of 3 consecutive i.p. injections of MTX. Tyrosine nitrated proteins and cysteine nitrosylated proteins were determined in the subcellular organelles fractions of mucosa using immunoprecipitation and western blot. The proteins in the subcellular fractions were separated by 1D electrophoresis, and probed with anti -nitrotyrosine antibody and anti-nitrosocysteine antibody. After MTX treatment, a general increase in protein tyrosine nitration as well as a change in the spectrum of proteins that underwent nitration was observed. The relative densities of the 3 nitrotyrosine protein adducts were as follows: Mitochondria > cytosol > microsomes > nucleus. In the mitochondrial fraction increased nitration of 12 kDa, 25 kDa 29Kda, 47 kDa, and 62Kda proteins, in the cytosol increased nitration of 12 kDa, 19 kDa, 45 kDa, and 60 kDa proteins and in the nuclear fraction increased nitration of 17 kDa, 35 kDa, and 58 kDa proteins was observed. On the other hand, MTX treatment resulted to a general decrease in protein cysteine nitrosylation in all the subcellular fractions. These results suggest that MTX induced, PON mediated small intestinal injury is mediated by differential nitration and nitrosylation of proteins in the subcellular organelles with increased protein tyrosine nitration and decreased cysteine nitrosylation. In addition MTX treatment results in selective nitration and nitrosylation of proteins in the intestinal mucosa. This differential nitrosative modifications may contribute to MTX induced small intestinal injury.

A study of the histological and functional changes of rat small intestinal mucosa in urinary circumstance

Objective To study the histological and functional changes of rat small intestinal mucosa in urinary circumstance for a long period. Methods 22 rats divided into two groups randomly, 12 rats in experiment group accepted bladder substitution operation use 4cm distal small intestine and 10 rats in control group accepted sham operation. 1 month and 5 month postoperation, to observe the histological changes, secretion and absorption changes of the neobladder mucosa, and body weight, blood biochemistry changes of the rats. Results 5 month postoperation, histological hyperplasia happened in neobladder mucosa.the number of goblet cells increased apparently 1 month postoperation and decreased significantly 5 month postoperation.neobladder mucosa showed absorption of water, K+ and NH+4, 1 h absorption were (0.39±0.09)ml,(5.2±0.9)μmol,(7.11±0.87)μmol, respectively;showed secretion of Na+, Cl-, HCO-3, 1 h secretion were(33.2±4.6),(8.0±3.7),(17.7±7.0)μmol, respectively, compared with the data obtained 1 month postoperation, the differences were not significant(P> 0.05).the weight of the residual mucus in the neobladder was(0.091±0.079)g,compared with the data obtained 1 month postoperation, the difference was significant(P 0.05). Conclusion After the rat small intestine mucosa is in contact with urine for a long period, the mucosa shows histological hyperplasia, the number of goblet cells increases in early period, and decreases in later period in this study; significant changes not happen in the mucosa absorption or secretion function of water and electrolyte; the weight of the residual mucus in the neobladder decrease gradually; using 4 cm distal segment of rat small intestine to form bladder substitute, not significantly effect on rat later stage healthy. Key words: Urinary diversion; Small intestinal mucosa

The effect of oat β‐glucan on in vitro glucose diffusion and glucose transport in rat small intestine

Many previous studies have reported the role of oat β-glucan (OBG) in the reduction of postprandial glucose, and hypothesised that OBG may form a protective layer along the intestinal wall, acting as a viscous barrier to decrease glucose transportation. This study examined whether the molecular weight (MW) and concentration of OBG affected the diffusion of glucose in vitro. The effect of OBG on glucose transportation in vitro and sodium-potassium adenosine triphosphatase (Na(+)/K(+)-ATPase) activity in the everted small intestines of normal rats was also examined. In vitro, higher MWs and concentrations of OBG increased the inhibitory effects on glucose diffusion and glucose adsorption. The transport of glucose by glucose transporters and Na(+)/K(+)-ATPase activity in the small intestinal mucosa of rats were significantly lower following the addition of OBG than those in the absence of OBG at the same time-points throughout glucose transportation (P < 0.05). In the OBG-treated group, the Na(+)/K(+)-ATPase activity decreased with increasing OBG MW. However, as the concentration of OBG in the solution increased, the Na(+)/K(+)-ATPase activity in the small intestine increased due to stronger gastrointestinal motility. We also found that higher MWs of OBG had a greater inhibitory effect on intestinal disaccharidase activities in vitro. Oat β-glucan is able to adsorb glucose molecules, inhibit glucose transport, decrease the concentration of available glucose and suppress disaccharidase activities in the small intestine.

The correlation between the expression of differentiation markers in rat small intestinal mucosa and the transcript levels of schlafen 3.

The normal absorptive function and structural maintenance of the intestinal mucosa depend on a constant process of proliferation of enterocytic stem cells followed by progressive differentiation toward a mature phenotype. The mechanisms that govern enterocytic differentiation in the mucosa of the small intestine are poorly understood. To determine whether schlafen 3 (but not other schlafen proteins) act in vivo and whether its effects are limited to the small intestine. We have previously demonstrated in nonmalignant rat intestinal IEC-6 cells that schlafen 3 levels correlate with the expression of various differentiation markers in vitro in response to differentiation stimuli. Randomized controlled experiment. Animal science laboratory. Male Sprague-Dawley rats 8 to 13 weeks old. Messenger RNA (mRNA) from jejunal and colonic mucosa was isolated, and transcript levels of schlafen proteins 1, 2, 3, 4, 5, 13, and 14; sucrase isomaltase (SI); dipeptidyl peptidase 4 (Dpp4); glucose transporter type 2 (Glut2); and villin were measured by quantitative reverse transcriptase-polymerase chain reaction. We tested parallel variations in protein levels by Western blotting and Dpp4 enzyme activity. The transcript level of schlafen 3 (Slfn3) correlated with the levels of the differentiation markers SI, Dpp4, Glut2, and villin. However, the expression of schlafen proteins 1, 2, 4, 5, 13, and 14 did not correlate with the expression of the differentiation markers. The mucosal mRNA levels of Slfn3, SI, Glut2, and Dpp4 were all substantially higher in the rat jejunum than in colonic mucosa by a mean (SE) factor of 51.0 (13.2) for 6 rats (P < .05), 599 (99) for 8 rats (P < .01), 12.5 (5.5) for 8 rats (P < .01), and 14.0 (3.9) for 8 rats (P < .01), respectively. In IEC-6 cells, infection with adenovirus-expressing GFP-tagged Slfn3 significantly increased Slfn3 expression and Dpp4-specific activity compared with GFP-expressing virus (in 6 rats; P < .05). Taken together with our previous in vitro observations, the results suggest that small intestinal enterocytic epithelial differentiation in rats may be regulated by Slfn3 in vivo, as in vitro, and that these effects may be specific to the small intestinal enterocytic phenotype as opposed to that of the mature colonocyte. Slfn3 human orthologs may be targeted to stimulate intestinal differentiation in patients with short bowel syndrome.

Berberine ameliorates COX-2 expression in rat small intestinal mucosa partially through PPARγ pathway during acute endotoxemia

Berberine hydrochloride (BBR), a plant alkaloid, has been used to treat intestinal inflammation or infection for years. Cyclooxygenase-2 (COX-2) is pro-inflammatory mediator and involved in the induction of gut inflammation. The expression of COX-2 in small bowel mucosa was determined and the mechanism by which BBR modulated COX-2 expression was explored in a rat model of endotoxemia induced by lipopolysaccharide (LPS). The results showed that without LPS stimulation COX-2 was constitutively expressed at low levels in control rats. LPS challenge rapidly induced COX-2 gene transcription resulting in high levels of inducible COX-2 expression in endotoxemic rats. BBR pre- and post-treatment had no marked effect on constitutive COX-2 expression but inhibited inducible COX-2 overexpression. LPS challenge increased the expression and phosphorylation of peroxisome proliferator-activated receptor gamma (PPARγ), p38 and activating transcription factor 2 and 3 (ATF2, ATF3), but the effects of LPS were inhibited by BBR treatment. GW9662 did not influence constitutive COX-2 expression but enhanced inducible COX-2 overproduction. Besides, GW9662 abolished the inhibitory effect of BBR on inducible COX-2, p38, ATF2, 3 expression and phosphorylation. Collectively, these results indicated that BBR gavage could attenuate the overexpression of inducible COX-2, not constitutive COX-2, in ileal mucosa during acute endotoxemia in part via activation of PPARγ pathway, which negatively interfered with p38/ATFs cascade.

Berberine hydrochloride attenuates cyclooxygenase-2 expression in rat small intestinal mucosa during acute endotoxemia

The effect of berberine hydrochloride (BBR) on inducible cyclooxygenase-2 (COX-2) in small intestinal mucosa and related mechanisms was investigated in a rat model of acute endotoxemia. The results showed that lipopolysaccharide (LPS) increased COX-2 expression, whereas SB202190 and BBR curtailed it. LPS increased phosphorylation of mucosal p38 MAPK and ATF2 as well as production of ATF2, whereas BBR attenuated these effects. LPS upregulated mucosal peroxisome proliferator-activated receptor gamma (PPARγ), but BBR reduced this receptor. GW9662 aggravated LPS-induced and reversed BBR-attenuated COX-2 expression. The findings showed that BBR ameliorated COX-2 overexpression partially via modulation of p38 and PPARγ pathways during acute endotoxemia.

Distribution of thiolated mucoadhesive nanoparticles on intestinal mucosa

It was the aim of the present study to evaluate and compare the distribution of thiolated mucoadhesive anionic poly(acrylic acid) (PAA) and cationic chitosan (CS) nanoparticles on intestinal mucosa. Modifications of these polymers were achieved by conjugation with cysteine (PAA–Cys) and 2-iminothiolane (CS–TBA). Nanoparticles (NP) were prepared by ionic gelation and labelled with the strong hydrophilic fluorescent dye Alexa Fluor 488 (AF 488) and hydrophobic fluorescein diacetate (FDA). Unmodified and modified CS and PAA NP were examined in vitro in terms of their mucoadhesive and mucus penetrating properties on the mucosa of rat small intestine. To investigate the transport of NP across the mucus layer, their diffusion behaviour through natural porcine intestinal mucus was studied through a new diffusion method developed by our group.Lyophilised particles displayed 526μmol/g (CS) and 513μmol/g (PAA) of free thiol groups and a zeta potential of 20mV (CS) and −14mV for PAA NP. Nanoparticle distribution on rat intestine suggested that mucoadhesion of thiolated NP is higher than the diffusion into the intestinal mucosa. Modified particles displayed more than a 6-fold increase in mucoadhesion compared to unmodified ones. The rank order with regard to mucoadhesion of all particles was: CS–TBA>PAA–Cys>CS>PAA, whereas CS–TBA showed 2-fold higher mucoadhesive properties compared to PAA–Cys NP. Diffusion through intestinal mucus was much higher for unmodified than for thiolated as well as for anionic compared to cationic particles. Overall, it was shown that thiolated particles of both anionic and cationic polymers have improved mucoadhesive properties and could be promising carriers for mucosal drug delivery.

Effects of octreotide on glucose transporter type 2 expression in obese rat small intestine

To investigate the effects of the somatostatin analogue, octreotide, on maltose and sucrase activities and expression of glucose transporter type 2 (GLUT2) in obese rat intestinal mucosa. We divided 49 Sprague-Dawley rats into a group of 31 high fat diet-induced obese rats and a group of 18 normal controls. The obese rats were separated into an octreotide treated group of 16 rats and an obese group of 15. The intervention group was injected with octreotide at 40 μg/kg body weight every 12 h for 8 d. Rat body weight was measured weekly to calculate Lee's index. After euthanization, maltase and sucrase activities in the small intestine were measured by activity assays, and the fasting plasma glucose level was measured. The expression of GLUT2 in small intestinal mucosa was analyzed by immunohistochemistry, reverse transcriptase polymerase chain reaction and Western blotting assays. Body weight, Lee's index, fasting plasma glucose level, maltase activity in small intestinal mucosa, mucosa and apical GLUT2, GLUT2 mRNA and protein expression levels were all significantly higher in the obese group than in the normal control group (605.61 ± 141.00 vs 378.54 ± 111.75, 337.61 ± 10.82 vs 318.73 ± 20.10, 8.60 ± 1.38 vs 7.33 ± 0.70, 156.01 ± 58.81 vs 50.43 ± 30.49, 390 744.2 ± 62 469.21 vs 170 546.50 ± 50 646.14, 26 740.18 ± 3809.60 vs 354.98 ± 57.19, 0.26 ± 0.11 vs 0.07 ± 0.02, and 2.08 ± 0.59 vs 1.27 ± 0.38, respectively, all P < 0.01). Sucrase activity did not differ between the two groups. Octreotide intervention significantly decreased the body weight and fasting plasma glucose level of obese rats (508.27 ± 94.39 vs 605.61 ± 141.00, 7.58 ± 1.51 vs 8.60 ±1.38, respectively, all P < 0.05). The intestinal mucosa and apical GLUT2, expression of GLUT2 mRNA and protein were also significantly lower in the octreotide intervention group than in the obese group (269 975.2 ± 53 730.94 vs 390 744.2 ± 62 469.21, 3758.06 ±364.51 vs 26 740.18 ± 3809.60, 0.08 ± 0.02 vs 0.26 ±0.11, and 1.31 ± 0.27 vs 2.08 ± 0.59, respectively, all P < 0.01). High fat diet-induced obesity is associated with elevated intestinal maltase activity, GLUT2 expression, and permanent apical GLUT2 in the small intestinal mucosa of rats. Octreotide can inhibit these effects.

Immunomodulatory effect of mushrooms on cytotoxic activity and cytokine production of intestinal lamina propria leukocytes does not necessarily depend on β-glucan contents

We evaluated the effects of seven mushroom extracts (Grifola frondosa, Pholiota nameko, Panellus serotinus, Hypsizygus marmoreus, Pleurotus cornucopiae, Armillaria mellea, and Flammulina velutipes) on cytotoxic activity and cytokine production of lamina propria leukocytes (LPLs) isolated from rat small (S) and large (L) intestinal mucosa. Boiling water extracts from seven species of mushrooms showed no direct cytotoxicity against the YAC-1 target cells. However, prominent increases of cytotoxicity were observed in S- and L-LPLs co-cultured with P. serotinus extract. Cytokine production (TNFα, IFNγ, IL-12 p70, and IL-4) of S- and L-LPLs was stimulated in response to P. cornucopiae extract. Mushroom extracts contributed to target cell adhesion and/or cytokine production in the effector cells. The promotion of cytotoxic activity in S- and L-LPLs was not necessarily related to β-glucan content of the mushroom.

The protective effects of intra-peritoneal fluid resuscitation on small intestinal mucosa in rats with hemorrhagic shock

Objective To investigate the protective effects of intra-peritoneal fluid resuscitation on small intestinal mucosa in rats with hemorrhagic shock. Method Fifty Sprague-Dawley (SD) rats were randomly (random number) divided into five groups, namely sham operation group (group I ), hemorrhagic shock group (group Ⅱ ), intra-venous fluid resuscitation group (group Ⅲ ) . intravenous fluid resuscitation plus intra-peritoneal saline resuscitation (group Ⅳ ) and intravenous fluid resuscitation plus intra-peritoneal PD-2 solution resuscitation group (group Ⅴ ). The rats of 5 groups were processed with cannulations of right common carotid artery, right femoral vein and left femoral artery with systemic heparinization. The rat models of hemorrhagic shock were established with modified Wigger' s method by which the blood exsanguinated from left femoral artery. The rats of group Ⅲ were resuscitated with shed blood plus twice equal volume of Ringer's solution after modeling of hemorrhagic shock.The rats of group Ⅳ and group Ⅴ were administered intra-peritoneally with 30 mL saline and 30 mL of 2.5% PD-2 solution, respectively as adjuncts to those used in the group Ⅲ . The specimens of blood and small intestine of rats of all groups were collected 60-120 minutes after modeling and resuscitation. The activity of plasma diamine oxidase (DAO) was determined with chromatometry, the level of plasma D-lactic acid (D-LA) with spectorophotometry and the level of plasma lipopolysaccharide (LPS) with nephelometry. The histopathological and ultrastructure changes of small intestine tissue of rats were observed under light microscope and electronic microscope. Results There were remarkable differences in activity of DAO, and the levels of D-LA and IPS in rats between those ingroup Ⅱ and group I (P <0.01), and between those in group V and groups Ⅱ , Ⅲ or Ⅳ (P <0.05 or P < 0.01) The pathomorphology and ultra-structure of small intestine tissues were severely damaged in group Ⅱ compared with those in group Ⅰ , and those markedly lessened in group V compared with groups Ⅱ , Ⅲ and Ⅳ . Conclusions Intraperitoneal fluid resuscitation with PD-2 solution can significantly protect the integrity of intestinal mucosa and the normal permeability of intestinal wall, and blunts the histopathological changes, and restrains bacterial translocation from gut and reduces the level of plasma endotoxin. Key words: Hemorrhagic shock; intestinal mucosa intraperitoneal resuscitation; bacterial translocation; multiple organ dysfunction syndrome; diamine oxidase; D-lactic acid; Lipopolysaccharide