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At least 847 records · Page 47Linked to original sources
PubMed1999

Radioprotection of the intestinal mucosa of rats by probucol.

Probucol is a lipid-regulating drug that also has antioxidant properties. This study was designed to test the possibility that probucol could provide radioprotection of the intestine when administered either intralumenally or systemically. Tissue damage was evaluated histologically by quantifying the number of crypts per circumference and the mucosal height. Animals were sacrificed 5 days after 11 Gy of X irradiation. In one series of experiments, a loop of mid small bowel was exteriorized operatively and compartmentalized into segments, each filled with probucol or saline. Intralumenal administration of probucol prior to irradiation led to a significantly greater number of crypts per circumference and mucosal height compared to saline-filled irradiated controls. In another series of experiments, five groups of rats were irradiated: (1) probucol in the small bowel lumen, (2) intravenous probucol, (3) probucol by gavage, (4) probucol added to standard rat chow and (5) saline control. In the rats given probucol intravenously prior to X irradiation, crypt numbers and mucosal height were significantly enhanced. Probucol given by gavage also resulted in protection. Rats fed a diet containing probucol showed no significant protection. Topical administration was more effective than systemic. Probucol protects the intestinal mucosa from acute radiation damage when given topically, intravenously or by gavage, but does not do so when given as a dietary supplement.

Animals↗
PubMed1993

Effects of sodium fluoride and cobalt chloride on the enantioselectivity of microsomal and cytosolic esterases in rat intestinal mucosa.

The effects of sodium fluoride (NaF) and cobalt chloride (CoCl2) on the enantioselective hydrolysis of racemic oxazepam 3-acetate (rac-OXA) by microsomal and cytosolic esterases in rat intestinal mucosa were studied. Microsomal and cytosolic esterases hydrolyzed S-OXA and R-OXA in approximately 1:19 and 4:1 ratios, respectively. The hydrolysis of R-OXA by microsomal esterases was inhibited by NaF with an IC50 of 13.4 +/- 1.5 mM. Hydrolyses of both S-OXA and R-OXA by cytosolic esterases were inhibited by NaF with a similar IC50 value (approximately 3 mM). The hydrolysis of S-OXA by cytosolic esterases was inhibited by CoCl2 (IC50 = approximately 5 mM), whereas the hydrolysis of R-OXA by cytosolic esterases was stimulated by approximately 10% in the presence of 1 mM CoCl2. In comparison, the hydrolysis of R-OXA by microsomal esterases was stimulated by approximately 55% in the presence of 1 mM CoCl2. These results not only revealed the effects of NaF and CoCl2 on the catalytic activities of enantioselective cytosolic and microsomal esterases, but also indicated that microsomal and cytosolic esterases that selectively hydrolyzed R-OXA were distinctly different protein entities.

Animals↗
PubMed1984

Prostaglandins in small intestinal mucosa of children with celiac disease.

Diarrhea is one of the important clinical symptoms in patients suffering from celiac disease and is attributed mainly to malabsorption. We determined prostanoid content in small intestinal mucosa of five patients with active celiac disease and in a control group consisting of six patients. Prostaglandin E2 and thromboxane B2 content in duodenal mucosa of patients with active celiac disease was 1,581 +/- 161 and 118 +/- 40 pg/mg wet wt, respectively, significantly higher than their content in duodenal mucosa of the control group, 378 +/- 86 and 8 +/- 8, p less than 0.001 and p less than 0.02, respectively. 6-Ketoprostaglandin F1 alpha content in celiac patients was not significantly different from its content in the control group: 908 +/- 437 and 124 +/- 53 pg/mg wet wt, respectively. It is possible that, in celiac disease, increased mucosal prostanoid content may contribute, at least in part, to intestinal electrolyte and fluid secretion and consequent diarrhea.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

[Regeneration of the gastric and intestinal mucosas].

The physiological cell renewal of gastrointestinal mucosa is regulated in man as in animal through certain mechanisms with measurable kinetic data. Pathologic mucosal alterations, metabolic disorders, pharmacological agents etc. clearly affect the regenerative processes of the gastrointestinal epithelium. Gastrin and pentagastrin stimulate the growth not only of the parietal cells, but also of the superficial epithelium of the gastric mucosa, whereas secretin does not change cell growth. Glucocorticoid steroids inhibit epithelial regeneration in all parts of the gastrointestinal tract. 5-fluorouracil has a similar effect but acts at a different site in the regeneration cycle. Epithelial cell proliferation of the gastric and intestinal mucosa is likewise inhibited in an uremic condition. In inflammatory changes in the human gastric mucosa epithelial cell hyperproliferation relative to the severity of gastritis and anomalous proliferation within regions of dysplasia can be demonstrated. Foveolary hyperplasia in Ménétrier's disease occurs on the basis of excessive hyperproliferation with displacement of regeneration zones.

Gastric Mucosa↗
PubMed1982

IgA-containing plasma cells in the intestinal mucosa of children with selective IgA deficiency.

In 8 children with selective IgA deficiency (serum IgA less than 5 mg/dl, secretory IgA less than 0.5 mg/dl in unstimulated saliva) immunofluorescent staining of intestinal biopsy specimens revealed the presence of IgA-containing plasma cells. This finding supports the hypothesis that in the intestinal mucosa of patients with IgA deficiency B lymphocytes undergo "sterile" differentiation into IgA-containing plasma cells probably incapable of secreting the IgA synthesized.

B-Lymphocytes↗
PubMed1991

Down-regulation of protein kinase C activation in human lamina propria T lymphocytes: influence of intestinal mucosa on T cell reactivity.

Human lamina propria T lymphocytes (LPL-T) were shown to have lower proliferative responses to CD3 triggering than autologous peripheral blood T lymphocytes (PBL-T), yet preserved their responsiveness to CD2 stimulation. In order to elucidate the basis of these differences, freshly recovered human LPL-T and autologous PBL-T were stimulated with CD2 monoclonal antibodies anti-T11(2/3) plus sheep red blood cells and phorbol 12,13-dibutyrate (PBu2) plus ionomycin, respectively. LPL-T showed invariably lower responses to PBu2 plus ionomycin than PBL-T. In contrast, LPL-T still preserved proliferation to CD2 activation even when their responses to PBu2 plus ionomycin were decreased almost to background levels. Preincubation of PBL-T with intestinal mucosa supernatant led to a similar reactivity as observed in fresh LPL-T. Moreover, the protein kinase C (PKC) inhibitor sphinganine was able to inhibit DNA synthesis to stimulation with PBu2 plus ionomycin but not to CD2 triggering. This study suggests that CD2-induced proliferation is not dependent on PKC activation and that down-regulation of PKC activation may be one of the mechanisms for inhibition of the CD3-Ti-dependent activation pathway in LPL-T by intestinal mucosa-derived influences in vivo.

Antigens↗
PubMed1981

[Animal experiments with ligation of intestinal segments to study absorption of alpha-amino-iso-butyric acid by intestinal mucosa of foetus (author's transl)].

The authors developed an animal model with ligation of intestinal segments of guinea pig foetuses. Evidence was found to the effect that amino acids were absorbed in high concentrations by foetal jejunum. A peculiar aspect, additionally detected, was relating to the capability of foetal intestinal mucosa to absorb large-molecular substances, such as inulin.

Aminobutyrates↗
PubMed1981

Effects of proteolytic enzymes on vitamin B12 uptake by rat intestinal mucosa homogenates and of proteolytic enzymes and anti-rat intrinsic factor antibodies on vitamin B12 absorption in total gastrectomized rats.

Trypsin inhibited 57CoB12-rat IF uptake by rat small intestinal mucosa homogenates in vitro. This tryptic inhibition was inactivated by rat serum and normal human serum, as well as soybean trypsin inhibitor (STI). The effects of trypsin dissolved in distilled water or 0.0025 N HCl, 0.15 M saline extract of rat pancreas and STI on vitamin B12 absorption were studied in vivo, using gastrectomized rats. IF-mediated B12 absorption was significantly decreased by 5 mg of trypsin dissolved either in distilled water or 0.0025 N HCl. However, the inhibition of trypsin was much more remarkable when it was dissolved in 0.0025 N HCl, whereas B12 absorption was insignificantly decreased by administering 10 mg of trypsin dissolved in 0.0025 N HCl. The possibilities of this phenomenon was discussed. The inhibitory effect of 0.5 ml of 0.15 M saline extract of rat pancreas was investigated as well. Soybean trypsin inhibition showed no effect on B12 absorption when it was given with 57CoB12-rat IF at the same time. However, the B12 absorption was significantly increased when STI was given one hour prior to the administration of 57CoB12-rat IF. This suggested that endogenous trypsin bound to rat small intestine had been inactivated and pancreatic secretion had been stimulated by STI. IF-mediated B12 absorption was diminished to almost the same level of 57CoB12 administration alone by simultaneous intubation of both 57CoB12-rat IF and rabbit anti-rat IF serum in total gastrectomized rats.

Animals↗
PubMedDate not supplied

Effects of the short-chain triglyceride triacetin on intestinal mucosa and metabolic substrates in rats.

Diets containing either triacetin (the water-soluble triglyceride of acetate) or long-chain triglycerides (LCTs) were fed to rats to determine the effects on intestinal mucosa cells and plasma substrates. Male Sprague-Dawley rats were fed one of three diets, a control diet containing 5% of energy as LCTs or one of two experimental diets that contained 30% of energy as lipid. The lipid component of the two experimental diets was either 100% LCTs or 95% triacetin/5% LCTs. Plasma lactate, glucose, and total ketone body concentrations were not significantly different among dietary treatment groups. Compared with animals fed LCTs and control diet, plasma pyruvate and free fatty acid concentrations were decreased in animals fed triacetin. In contrast, plasma triglyceride concentrations were elevated in animals fed triacetin compared with other groups. Intestinal biochemical measures included total DNA, RNA, protein, and the protein:DNA ratio. Histologic indices measured were villus height in the jejunum and crypt depth in the colon. No significant difference in mucosal protein concentration was observed in the jejunum and colon. Jejunal RNA was significantly decreased in animals fed triacetin compared with other diets. Triacetin feeding significantly increased the DNA content in the jejunum and colon (thereby lowering the protein:DNA ratio), indicating smaller, more numerous cells. Jejunal villus height and colonic crypt depth were not significantly different among dietary treatment groups. Provision of a balanced diet containing 28.5% of the total calories as triacetin had no adverse effects on metabolic substrates and resulted in smaller and more numerous mucosal cells in the jejunum and colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Identification of a T cell lymphoma category derived from intestinal-mucosa-associated T cells.

2 cases of precursor T cell lymphoma and 37 cases of peripheral T cell lymphoma were investigated for their reactivity with the monoclonal antibody (mAb) HML-1, which recognises human intestinal T lymphocytes but not lymph-node T cells. In all but one of the lymphomas studied, the tumour cells were unreactive with the mAb HML-1. The HML-1+ lymphoma was the only tumour that was primarily localised in the epithelium and lamina propria of the small intestine, and was associated with ulcerative jejunitis and coeliac disease. This result suggests that the HML-1+ lymphoma was derived from intestinal mucosa T lymphocytes and differs from precursor T cell lymphoblastic lymphomas and nodal and cutaneous peripheral T cell lymphomas.

Aged↗