13 research outputs found
Novel features of the rat model of inflammatory bowel disease based on 2,4,6-trinitrobenzenesulfonic acidinduced acute colitis
The 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute inflammatory bowel disease (IBD) model in the rat is discussed, focusing on the details of the TNBS instillation and highlighting the advantages and limitations of this model. For determination of the time-dependent action of 50% ethanol and different doses of TNBS, male Wistar rats were treated with 50% ethanol or 10 mg or 30 mg of TNBS dissolved in 50% ethanol. The TNBS-induced inflammation peaked 48-72 h after installation and the colitis caused by 30 mg of TNBS was more severe than that caused by 10 mg of TNBS. To test the effectiveness of sulfasalazine (SASP), male rats were treated with 10 mg of TNBS or with 10 mg of TNBS and SASP, and 72 h later the extent of mucosal damage was determined. Orally administered 50 mg/kg/day SASP proved to reduce the TNBS-induced colonic inflammation in rats significantly. The TNBS-induced colitis model facilitates a better understanding of the immunopathological mechanisms of IBD. Optimization of the dose of TNBS and oral SASP as positive control in TNBS-induced colitis in rats furnishes an appropriate test system for new anti-IBD drugs
Segregation of granular binary mixtures by a ratchet mechanism
We report on a segregation scheme for granular binary mixtures, where the
segregation is performed by a ratchet mechanism realized by a vertically shaken
asymmetric sawtooth-shaped base in a quasi-two-dimensional box. We have studied
this system by computer simulations and found that most binary mixtures can be
segregated using an appropriately chosen ratchet, even when the particles in
the two components have the same size, and differ only in their normal
restitution coefficient or friction coefficient. These results suggest that the
components of otherwise non-segregating granular mixtures may be separated
using our method.Comment: revtex, 4 pages, 4 figures, submitte
Novel features of the rat model of inflammatory bowel disease based on 2,4,6-trinitrobenzenesulfonic acid - induced acute colitis
The 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute inflammatory bowel disease (IBD) model in the rat is discussed, focusing on the details of the TNBS instillation and highlighting the advantages and limitations of this model. For determination of the time-dependent action of 50% ethanol and different doses of TNBS, male Wistar rats were treated with 50% ethanol or 10 mg or 30 mg of TNBS dissolved in 50% ethanol. The TNBS-induced inflammation peaked 48-72 h after installation and the colitis caused by 30 mg of TNBS was more severe than that caused by 10 mg of TNBS. To test the effectiveness of sulfasalazine (SASP), male rats were treated with 10 mg of TNBS or with 10 mg of TNBS and SASP, and 72 h later the extent of mucosal damage was determined. Orally administered 50 mg/kg/day SASP proved to reduce the TNBS-induced colonic inflammation in rats significantly. The TNBS-induced colitis model facilitates a better understanding of the immunopathological mechanisms of IBD. Optimization of the dose of TNBS and oral SASP as positive control in TNBS-induced colitis in rats furnishes an appropriate test system for new anti-IBD drugs
Ghrelin-Induced Enhancement of Vasopressin and Oxytocin Secretion in Rat Neurohypophyseal Cell Cultures
The effects of ghrelin on vasopressin and oxytocin secretion
were studied in 13-14-day cell cultures of isolated rat
neurohypophyseal tissue. The vasopressin and oxytocin
contents of the supernatant were determined by
radioimmunoassay after a 1- or 2-h incubation. Significantly
increased levels of vasopressin and oxytocin production were
detected in the cell culture media following ghrelin
administration, depending on the ghrelin doses. The oxytocin
level proved to be more elevated than that of vasopressin.
The increase of vasopressin and oxytocin secretion could be
totally blocked by previous administration of the ghrelin
receptor antagonist ([D-Lys3]-growth hormone-releasing
peptide-6). Application of the ghrelin receptor antagonist
after ghrelin administration proved ineffective. The results
indicate that vasopressin and oxytocin release is influenced
directly by the ghrelin system, and the effects of ghrelin on
vasopressin and oxytocin secretion from the neurohypophyseal
tissue in rats can occur at the level of the posterior
pituitary. Our observations lend support to the view that
neurohypophysis contains ghrelin receptors
Keto-Enol-Tautomerie und das Dipolmoment des Assoziats im Cyclohexanon-Tetrachlorkohlenstoff-Gemisch
New Metabolic Influencer on Oxytocin Release: The Ghrelin
Background: The hypothalamic–pituitary axis by secreting neuropeptides plays a key role in metabolic homeostasis. In light of the metabolic regulation, oxytocin is a potential neuropeptide for therapies against obesity and related disorders. The aim of our study is to measure ghrelin-induced oxytocin secretion in rats and to detect the changes after administration of ghrelin antagonist. Methods: Ghrelin was administrated centrally (intracerebroventricular, i.c.v., 1.0, 10.0, and 100.0 pmol) or systemically (intravenous, i.v., 1.0, and 10.0 nmol). [d-Lys3]-GHRP-6 ghrelin antagonist was injected 15 min before ghrelin injection in a dose of 10.0 pmol i.c.v. and 10.0 nmol i.v. Results: Either i.c.v. or i.v. administration of ghrelin dose-dependently increased the plasma oxytocin concentration. Following pretreatment with the ghrelin antagonist [d-Lys3]-GHRP-6, the high plasma oxytocin level induced by ghrelin was significantly reduced. Conclusion: The results indicate that the release of oxytocin is influenced directly by the ghrelin system. Examination of the mechanism of ghrelin-induced oxytocin secretion is a new horizon for potential therapeutic options