Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of foreign gastroenterologists have their doubts whether there exist "undifferentiated" colitisis. They consider these to be a variant of the irritable bowel syndrome. We have examined 173 patients. Of these, 67 percent were less than 45 years of age with significant intestinal disorders caused by chronic colitis. Diagnosis of Crohn's disease and nonspecific ulcerative colitis had been excluded. The main complaints of the patients were constipations alternated sometimes with short-time diarrhea (61%), diarrhea (13%), spasmodic pains in the inferior parts of the abdomen (20%), abdominal distention, and rumbling (74%). In 79% there was tenderness in the sygmoid colon and caecum and spasm thereof. Rectoromanoscopy (RRS) revealed normal mucosa of the rectum and sygmoid colon in 70%, proctosygmoiditis (predominantly catarrhal) in 30 percent of cases. In proctosygmoiditis (vs the normal mucosa) motor dysfunctions, disorders of the contrast mass passage through the intestine, gaustrations were more often seen but the relief of the mucosa was intact. Results of morphological investigations of biopsy specimens of rectal and sygmoidal mucosas were compared with endoscopy findings. No histological changes were revealed in 23% patients with proctosygmoiditis whereas in cases of endoscopically normal mucosa moderate inflammation was rarely detectable. Inflammatory changes in the mucosa were to be seen more frequently by cytologic analysis than by biopsy but more rarely than by RRS. In this way, 25% patients with endoscopical diagnosis of proctosygmoiditis had normal cytological picture. The increased amount of intestinal enzymes (enterokynase, alkaline phosphatase) in stools does not permit differentiating the functional and organic types of the disease, but it significantly contributes to endoscopical, morphological, cytological, and clinical data. Our investigations show that "undifferentiated" colitis is a rarity and that one finds difficulty in differentiating between the above condition and the irritable bowel syndrome.
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PMID:[Differential diagnosis in "undifferentiated" inflammatory diseases and dyskinesias of the large intestine]. 1188 61

Quercitrin is a flavonoid with antiinflammatory activity in experimental colitis, associated with an antioxidative action and amelioration of water absorption in vivo. However, its mechanism of action is unclear. This study focuses on the effect of quercitrin (1 and 5 mg/kg) in the early stages (24 h) of trinitrobenzene sulfonic acid colitis. Treatment with the flavonoid prevented the increase in colonic malondialdehyde and inhibited nitric oxide synthase and alkaline phosphatase activity but had no significant effects on observable damage. No effect on neutrophil infiltration (myeloperoxidase) was observed. On the other hand, quercitrin exerted complex effects on colonic hydroelectrolytic transport, showing a slight potentiation of water absorption in vivo (5 mg/kg) as well as a normalization of carbachol stimulated electrogenic ionic transport in the proximal colon in vitro (5 mg/kg). It is concluded that the beneficial effects of quercitrin on trinitrobenzene sulfonic acid chronic colitis arise from an early downregulation of the inflammatory cascade that is associated with amelioration of the disturbances in hydroelectrolytic transport.
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PMID:Effect of quercitrin on the early stages of hapten induced colonic inflammation in the rat. 1200 93

In the present study, we aimed to investigate enterocyte- and goblet cell-specific functions during the different phases of acute colitis induced with dextran sulfate sodium (DSS). Rats were treated with DSS for 7 days, followed by a 7-day recovery period. Colonic tissue was excised on days 2 (onset of disease), 7 (active disease), and 14 (regenerative phase). Enterocyte functions were studied by the expression of carbonic anhydrases (CAs), sodium/hydrogen exchangers (NHEs) and intestinal fatty acid-binding protein (iFABP) and by alkaline phosphatase (AP) activity. The expression and secretion of the mucin Muc2 and trefoil factor family peptide-3 (TFF3) were used as parameters for goblet cell function. DSS induced a downregulation of the CAs, NHEs, and iFABP in some normal-appearing surface enterocytes and in most of the flattened-surface enterocytes during disease onset and active disease. During the regenerative phase most enterocytes expressed these genes again. Quantitative analysis revealed a significant decrease in CAs, NHEs, and iFABP expression levels during onset and active disease. During the regenerative phase, the expression levels of the CAs were restored, whereas the expression levels of the NHEs and iFABP remained decreased. In contrast, enterocyte-specific AP activity was maintained in normal and flattened enterocytes during DSS-induced colitis. Goblet cells continued to express MUC2 and TFF3 during and after DSS treatment. Moreover, Muc2 and TFF3 expression and secretion levels were maintained or even increased during each of the DSS-induced disease phases. In conclusion, DSS-induced colitis was associated with decreased expression of CAs, NHEs, and iFABP. The loss of these genes possibly accounts for some of the pathology seen in colitis. The maintenance or upregulation of Muc2 and TFF3 synthesis and secretion levels implies that goblet cells at least maintain their epithelial defense and repair capacity during acute inflammation induced by DSS.
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PMID:Distinct epithelial responses in experimental colitis: implications for ion uptake and mucosal protection. 1206 4

It is unknown why some patients with inflammatory bowel disease develop primary sclerosing cholangitis. We have recently shown that patients with primary sclerosing cholangitis have an increased prevalence of mutations in the gene responsible for cystic fibrosis (CFTR) compared with individuals with inflammatory bowel disease alone. Our aim was to examine whether induction of colitis by oral dextran leads to bile duct injury in mice heterozygous or homozygous for mutations in CFTR. The effect of oral administration of docosahexaenoic acid to correct a fatty acid imbalance associated with cystic fibrosis was also examined to determine whether this would prevent bile duct inflammation. Wild-type mice and mice heterozygous and homozygous for CFTR mutations were given dextran orally for 14 days to induce colitis. Bile duct injury was quantitated by blinded histological scoring and measurement of serum alkaline phosphatase activity. The effect of pretreatment with docosahexaenoic acid for 7 days was examined. Treatment of mice with 100 mg dextran/day for 9 days followed by 85 mg/day for 5 days resulted in a significant increase in bile duct injury as determined by histological scoring in homozygous cystic fibrosis mice compared with wild-type mice (P = 0.005). The bile duct injury seen in cystic fibrosis mice was reflected in a threefold increase in serum alkaline phosphatase (P = 0.0006). Pretreatment with oral docosahexaenoic acid decreased both histological evidence of bile duct injury and serum alkaline phosphatase levels. In the setting of colitis, loss of CFTR function leads to bile duct injury.
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PMID:Induction of colitis in cftr-/- mice results in bile duct injury. 1506 32

This study demonstrates the upregulation of alkaline phosphatase and the mechanisms involved in experimental colitis. All models of ileal and colonic inflammation examined, which were characterized by significant oxidative stress and neutrophil infiltration, resulted in an increase in alkaline phosphatase activity which was attributable to both epithelial cells and cells of the lamina propria, mainly leukocytes. The increase in alkaline phosphatase sensitivity to the inhibitors levamisole and homoarginine, together with changes in the apparent molecular size and in the sialization of the enzyme, indicated a change in the isoform expressed. An increase in tissue non-specific alkaline phosphatase expression was observed by Western blotting. Treatment with the bone/kidney alkaline phosphatase inhibitor levamisole or a monoclonal antibody resulted in significant protection from colonic inflammation. Taken together, these results indicate that the kidney isoform is a marker of intestinal inflammation and that it might even constitute a target for pharmacological intervention.
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PMID:Induction of alkaline phosphatase in the inflamed intestine: a novel pharmacological target for inflammatory bowel disease. 1554 78

Monochloramine is a powerful oxidative molecule that is produced in inflammatory sites. We investigated the effect of intrarectally administered monochloramine (3.2 mg) in the rat. A single enema induced after 24 h an intense inflammatory reaction characterized by mucosal necrosis, submucosal edema, hemorrhage and colonic thickening, as well as induction of nitric oxide synthase and tumor necrosis factor and an increase in the interferon gamma/interleukin 4 ratio. The inflammatory response peaked 3-5 days after monochloramine administration and then followed a extended recovery phase. At 1 week there was substantial but incomplete mucosal repair, submucosal edema, neutrophil/macrophage infiltration and increased myeloperoxydase and alkaline phosphatase activities. Oxidative stress, as determined by malonyldialdehyde levels, was prominent only in the acute phase (3-5 days). Monochloramine colitis was amenable to pharmacological treatment with sulphasalazine or prednisolone, suggesting that it may be used as an experimental model of inflammatory bowel disease. In conclusion, monochloramine induces acute and protracted colonic inflammation in the rat. Locally produced monochloramine might contribute to the perpetuation of inflammatory bowel disease.
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PMID:Monochloramine induces acute and protracted colitis in the rat: response to pharmacological treatment. 1582 May 7

Milk kappa-casein-derived glycomacropeptide has immunomodulatory and bacterial toxin binding effects. The intestinal anti-inflammatory activity of glycomacropeptide was assessed in trinitrobenzenesulfonic acid-induced colitis in rats. Rats were administered glycomacropeptide daily starting either 2 d before (pretreatment) or 3 h after (post-treatment) colitis induction. Pretreatment with glycomacropeptide had a dose-dependent anti-inflammatory effect, characterized by lower body weight loss, decreased anorexia (57%), colonic damage (65%), and weight to length ratio (32%), as well as a reduction in colonic alkaline phosphatase activity (42%) and interleukin 1, trefoil factor 3, and inducible nitric oxide synthase mRNA levels (P < 0.05). The mechanism of action of glycomacropeptide is unknown but is consistent with an inhibition of the activation of immune cells. The magnitude of the anti-inflammatory effect was generally comparable to that of sulfasalazine, an established drug used in the treatment of inflammatory bowel disease. Bovine glycomacropeptide may play a role in the management of patients with inflammatory bowel disease.
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PMID:Bovine glycomacropeptide is anti-inflammatory in rats with hapten-induced colitis. 1586 98

An asymptomatic, but highly significant, rise in serum alkaline phosphatase (AP) levels developed in a renal transplant recipient. Investigations ruled out bony or hepatobiliary disease. Subsequent diarrhea and weight loss led to a diagnosis of cytomegalovirus (CMV) colitis, which was confirmed with a positive CMV pp65 antigenemia test and an endoscopic finding of multiple colonic erosions. Intravenous ganciclovir led to complete patient recovery and a swift reduction of serum AP levels to normal. Normally, intestinal AP isoenzymes are cleared quickly from the circulation. However, acute bowel diseases, especially when inflammatory in origin, can produce high serum AP levels. In this presented patient, the rise in serum AP levels preceded symptomatic manifestations of CMV colitis, and fell with successful therapy. Acute CMV disease in solid organ transplant recipients is common, can take many shapes, and needs to be diagnosed quickly. An unexplained rise in serum AP levels should lead to a search for inflammatory bowel disease, specifically CMV colitis, in transplanted patients.
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PMID:Elevated serum alkaline phosphatase levels in a renal transplant patient precede colitis. 1691 74

Low-molecular-weight heparins (LMWH) have been shown to be efficient in the treatment of inflammatory bowel disease (IBD). Parenteral heparin therapy, however, may cause hemorrhagic adverse effects. To reduce this risk, epithelial LMWH delivery in combination with a system ensuring selective drug release to the inflamed tissue was tested here. Enoxaparin loaded microspheres (MS) were administered orally to male BALB mice suffering from a pre-existing experimental colitis, whereas control groups received subcutaneous or rectal LMWH solution. Colon weight/length index and alkaline phosphatase and myeloperoxidase activities were assessed to determine the inflammation. Tissue penetration experiments elucidated the processes involved in the proposed new therapeutic approach. Oral LMWH-MS proved to be equally efficient in mitigating experimental colitis as rectally administered LMWH solution when quantified by myeloperoxidase activity (MS, 10.2+/-1.5 U/mg tissue; rectal, 9.2+/-1.6 U/mg) and to be superior to subcutaneous LMWH (s.c., 21.6+/-5.6 U/mg; untreated colitis control, 30.0+/-3.8 U/mg). Pharmacokinetic studies found a notably low systemic availability of oral LMWH delivered from MS (<5%) indicating a low potential for adverse effects. The tissue permeability was selectively enhanced in the inflamed regions where a 9-fold higher LMWH penetration was found compared with healthy tissue. Epithelial LMWH delivery has been found a promising anti-inflammatory therapeutic approach. The use of LMWH-MS in this context offers a promising tool for IBD therapy by enhancing specifically drug availability at inflamed tissue sites while reducing the risk for systemic adverse effects to a negligibly low level.
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PMID:Epithelial heparin delivery via microspheres mitigates experimental colitis in mice. 1732 27

Active hexose correlated compound (AHCC) is a product prepared from the mycelium of edible Basidiomycete fungi that contains oligosaccharides. Here we have studied the antiinflammatory effect of AHCC in the trinitrobenzenesulfonic acid (TNBS) model of colitis in rats. Rats received AHCC (100 or 500 mg/kg) daily starting 2 d before (pretreatment) colitis induction and were killed 6 d after the TNBS challenge. The status of the rats was assessed by morphological and biochemical methods. The effect of AHCC on the colonic microflora was also assessed by studying the bacteria profile in feces by standard culture techniques. AHCC administration attenuated colonic inflammation, improving rat weight, food intake, damage score, extension of necrosis, colonic weight, colonic weight-to-length ratio, myeloperoxidase and alkaline phosphatase activities, glutathione concentration, and the expression of proinflammatory cytokines and chemokines (IL-1beta, IL-1 receptor antagonist, TNF, and monocyte chemoattractant protein-1) and of mucins 2-4 and trefoil factor 3. The magnitude of the antiinflammatory effect of AHCC was similar to that of sulfasalazine (200 mg/kg). The study of colonic microflora indicated that rats treated with AHCC had higher aerobic and lactic acid bacteria counts as well as higher bifidobacteria counts, whereas clostridia were reduced when compared with the TNBS group. Therefore, our results indicate that AHCC is antiinflammatory and could be useful as a prebiotic to design functional foods for inflammatory bowel disease patients.
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PMID:Active hexose correlated compound acts as a prebiotic and is antiinflammatory in rats with hapten-induced colitis. 1744 85


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