Home About us Contact
|
Home About us Contact | ||
|
|
||
Rat Colon (rat + colon)
Terms modified by Rat Colon Selected AbstractsThe Secretory Response of the Rat Colon to the Flavonol Quercetin is Dependent on Ca2+ -CalmodulinEXPERIMENTAL PHYSIOLOGY, Issue 3 2000R. Cermak The dietary flavonol quercetin induces chloride secretion in rat intestine. To clarify the underlying mechanisms, experiments were performed in Ussing chambers with tissue from rat proximal and distal colon. Quercetin induced an increase in short-circuit current (Isc), which was largely independent of submucosal neurons, as it was not affected by the neurotoxin tetrodotoxin. The effect of quercetin was blocked by the calmodulin antagonists trifluoperazine and ophiobolin A and was diminished by a blocker of Ca2+ release from intracellular stores (TMB-8), whereas the muscarinic receptor antagonist atropine was ineffective. The quercetin-induced Isc was abolished in Ca2+ -free solution. The flavonol was able to further increase Isc after maximal stimulation of the cAMP pathway by forskolin. The Isc increase by the flavonol was differently affected by two analogous phosphodiesterase inhibitors. Whereas 3-isobutyl-1-methylxanthine (IBMX) antagonized the effect of quercetin, 8-methoxymethyl-IBMX had no effect. Both phosphodiesterase inhibitors similarly influenced the Isc increase induced by forskolin. These results indicate that the chloride secretion induced by quercetin in rat colon depends on Ca2+ and calmodulin. The cAMP pathway and inhibition of phosphodiesterase appear not to be responsible for the secretory activity of the flavonol. [source] Prostaglandin I2 sensory input into the enteric nervous system during distension-induced colonic chloride secretion in rat colonACTA PHYSIOLOGICA, Issue 3 2010J. D. Schulzke Abstract Aim:, Intestinal pressure differences or experimental distension induce ion secretion via the enteric nervous system, the sensorial origin of which is only poorly understood. This study aimed to investigate sensorial inputs and the role of afferent and interneurones in mechanically activated submucosal secretory reflex circuits. Methods:, Distension-induced rheogenic chloride secretion was measured as increase in short-circuit current 10 min after distension (,ISC10; distension parameters ± 100 ,L, 2 Hz, 20 s) in partially stripped rat distal colon in the Ussing-chamber in vitro. PGE2 and PGI2 were measured by radioimmunoassay. Results:, ,ISC10 was 2.0 ± 0.2 ,mol h,1 cm,2 and could be attenuated by lobeline, mecamylamine and dimethylphenylpiperazine, indicating an influence of nicotinergic interneurones. Additionally, a contribution of afferent neurones was indicated from the short-term potentiation of ,ISC10 by capsaicin (1 ,m). As evidence for its initial event, indomethacin (1 ,m) inhibited distension-induced secretion and the release of PGI2 was directly detected after distension. Furthermore, serotoninergic mediation was confirmed by granisetron (100 ,m) which was functionally localized distally to PGI2 in this reflex circuit, as granisetron inhibited an iloprost-induced ISC, while indomethacin did not affect serotonin-activated ion secretion. Conclusions:, Distension-induced active electrogenic chloride secretion in rat colon is mediated by a neuronal reflex circuit which includes afferent neurones and nicotinergic interneurones. It is initiated by distension-induced PGI2 release from subepithelial cells triggering this reflex via serotoninergic 5-HT3 receptor transmission. Functionally, this mechanism may help to protect against intestinal stasis but could also contribute to luminal fluid loss, e.g. during intestinal obstruction. [source] Modifying effect of propolis on dimethylhydrazine-induced DNA damage but not colonic aberrant crypt foci in ratsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2005Rodrigo O. Alves de Lima Abstract Propolis is a honeybee product with several biological and therapeutic properties, including antimutagenic and anticarcinogenic activities. The effects of an aqueous extract of propolis (AEP) were evaluated on the formation of 1,2-dimethylhydrazine (DMH)-induced aberrant crypt foci (ACF) and DNA damage in the colon of male Wistar rats by the ACF and Comet assays, respectively. AEP was administered orally at 0.01%, 0.03%, 0.1%, and 0.3% in the drinking water, which resulted in doses of approximately 12, 34, 108, and 336 mg/kg body weight/day. Animals were also given a single subcutaneous injection of 40 mg/kg DMH and sacrificed 4 hr later for evaluating DNA damage, or 4 doses of 40 mg/kg DMH, administered 2 doses/week for 2 weeks, and sacrificed 12 weeks after the last injection for evaluating ACF development in the distal colon. Administration of AEP either simultaneously with or after the DMH treatment resulted in no statistically significant reduction of ACF. In contrast, 0.01%, 0.03%, and 0.3% AEP, given simultaneously with DMH, reduced DNA damage induction in the mid and distal colon. However, 0.3% AEP alone increased DNA damage in the colon. In conclusion, AEP had no effect on the formation of DMH-induced ACF in rat colon, but it modulated DMH-induced DNA damage in colon cells. Further investigations are recommended in order to establish the conditions under which propolis produces either protective or deleterious effects. Environ. Mol. Mutagen., 2005. © 2004 Wiley-Liss, Inc. [source] The Secretory Response of the Rat Colon to the Flavonol Quercetin is Dependent on Ca2+ -CalmodulinEXPERIMENTAL PHYSIOLOGY, Issue 3 2000R. Cermak The dietary flavonol quercetin induces chloride secretion in rat intestine. To clarify the underlying mechanisms, experiments were performed in Ussing chambers with tissue from rat proximal and distal colon. Quercetin induced an increase in short-circuit current (Isc), which was largely independent of submucosal neurons, as it was not affected by the neurotoxin tetrodotoxin. The effect of quercetin was blocked by the calmodulin antagonists trifluoperazine and ophiobolin A and was diminished by a blocker of Ca2+ release from intracellular stores (TMB-8), whereas the muscarinic receptor antagonist atropine was ineffective. The quercetin-induced Isc was abolished in Ca2+ -free solution. The flavonol was able to further increase Isc after maximal stimulation of the cAMP pathway by forskolin. The Isc increase by the flavonol was differently affected by two analogous phosphodiesterase inhibitors. Whereas 3-isobutyl-1-methylxanthine (IBMX) antagonized the effect of quercetin, 8-methoxymethyl-IBMX had no effect. Both phosphodiesterase inhibitors similarly influenced the Isc increase induced by forskolin. These results indicate that the chloride secretion induced by quercetin in rat colon depends on Ca2+ and calmodulin. The cAMP pathway and inhibition of phosphodiesterase appear not to be responsible for the secretory activity of the flavonol. [source] Endogenous endothelin in a rat model of acute colonic mucosal injuryJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2000Masamitsu Sugimachi Abstract Background: Endothelin (ET) is involved in various biologic activities in non-vascular and vascular tissues. While ET has some significant effects on gastrointestinal functions, the possible role of endogenous ET in the host response to mucosal injury has not been well clarified. Methods: The present study describes an investigation of the effects of an endothelin A receptor antagonist, BQ-123, on lactate dehydrogenase (LDH), mucus and albumin flux into the perfusate in a rat model of acute colonic injury, induced by acetic acid perfusion. The present study also examined localization of ET in damaged rat colons by using immunohistochemistry. Results: A 4% acetic acid treatment induced mild mucosal damage of perfused rat colon and increased LDH as well as albumin and protein-bound hexose release into the perfusate. Pretreatment with BQ-123 significantly reduced LDH activity and protein-bound hexose concentration in the perfusate and delayed the reduction of albumin leakage from damaged mucosa. Vascular endothelial, neural and surface epithelial cells of the colon showed strong ET-like immunoreactivity. Mucosal damage markedly influenced ET expression by epithelial cells. Mild mucosal damage decreased the ET expression by surface epithelial cells while moderate mucosal damage induced a mosaic location of ET-positive epithelial cells in the crypt. Severe mucosal damage abolished the ET expression by epithelial cells. Conclusions: Endothelin may play a role in the host response to acute mucosal damage. Mucosal ET production is significantly affected by mucosal injury. [source] Selective ,1 -adrenoreceptor blocking activity of newly synthesized acyl amino-substituted aryloxypropanolamine derivatives, DPJ 955 and DPJ 890, in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2005K. Nandakumar The in-vivo ,-adrenoreceptor antagonistic activity of test compounds DPJ 955 and DPJ 890 was assessed against ,-adrenoreceptor agonist (isoprenaline) induced tachycardia in anaesthetized rats. The selectivity to block isoprenaline responses on different ,-adrenoreceptor subtypes (,1, ,2 and ,3) of the test compounds was carried out on isolated rat right atria, isolated rat uterus and isolated rat colon preparations, respectively. Intravenous injection of isoprenaline alone in anaesthetized rats caused hypotension and tachycardia. DPJ 955 or DPJ 890 alone produced a fall in mean arterial pressure and bradycardia in a dose-dependent manner. Administration of isoprenaline to anaesthetized rats pre-treated with test compounds significantly blocked both the tachycardial and hypotensive responses induced by isoprenaline. The test compounds shifted the concentration response curves of isoprenaline towards the right for isolated rat right atrial preparations, rat uterus and rat colon, indicating ,1, ,2 and ,3 adrenoreceptor blockade, respectively. The selectivity ratio for ,1/,-adrenoreceptors to DPJ 955 and DPJ 890 was 64.6 and 83.2, respectively. DPJ 890 was more potent in blocking ,1 -adrenoreceptors and was more selective towards ,1 receptors than to other ,-adrenoreceptor subtypes. In conclusion, DPJ 955 and DPJ890 have ,-adrenoreceptor blocking activity with high selectivity for the ,1 -adrenoreceptor subtype. [source] Antioxidative capacity produced by Bifidobacterium - and Lactobacillus acidophilus -mediated fermentations of konjac glucomannan and glucomannan oligosaccharidesJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 7 2008Cheng-Hsin Wang Abstract BACKGROUND: Konjac glucomannan (KGM) has been shown to stimulate the growth of bifidobacteria and lactobacilli in the human and rat colon. This study investigated the antioxidative effects produced after 48 h in vitro fermentation of unhydrolysed KGM and two hydrolysed KGM fractions (KH1 and KH2 with degree of polymerisation 10 and 5 respectively) by Bifidobacterium adolescentis, B. bifidum, B. breve, B. longum and Lactobacillus acidophilus respectively. The inhibitory effect on conjugated diene formation, ferric-chelating capacity, ,,,-diphenyl-,-picrylhydrazyl (DPPH) radical-scavenging ability and thiobarbituric acid-reactive substances (TBARS) concentration produced by these fermentations were compared with those of oligofructose (OF) fermentation. RESULTS: The fermentation of KGM by each bacterial strain produced higher ferric-chelating capacity of the culture supernatant compared with KH2 or OF fermentation. In contrast, the fermentation of KGM by each bacterial strain led to lower inhibition of conjugated diene formation and lower radical-scavenging ability compared with KH2 fermentation. The fermentation of KH2 produced the lowest amount of TBARS. CONCLUSION: The fermentation of unhydrolysed KGM by colonic lactic acid bacteria in vitro produced antioxidative capacity mainly by preventing the initiation of ferrous ion-induced peroxidation, whereas the fermentation of konjac oligosaccahrides did so by increasing the radical-scavenging ability and eliminating lipid peroxide formation. Copyright © 2008 Society of Chemical Industry [source] The effect of naloxone-3-glucuronide on colonic transit time in healthy men after acute morphine administration: a placebo-controlled double-blinded crossover preclinical volunteer studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11-12 2008P. NETZER Summary Background, Constipation is a significant side effect of opioid therapy. We have previously demonstrated that naloxone-3-glucuronide (NX3G) antagonizes the motility-lowering-effect of morphine in the rat colon. Aim, To find out whether oral NX3G is able to reduce the morphine-induced delay in colonic transit time (CTT) without being absorbed and influencing the analgesic effect. Methods, Fifteen male volunteers were included. Pharmacokinetics: after oral administration of 0.16 mg/kg NX3G, blood samples were collected over a 6-h period. Pharmacodynamics: NX3G or placebo was then given at the start time and every 4 h thereafter. Morphine (0.05 mg/kg) or placebo was injected s.c. 2 h after starting and thereafter every 6 h for 24 h. CTT was measured over a 48-h period by scintigraphy. Pressure pain threshold tests were performed. Results, Neither NX3G nor naloxone was detected in the venous blood. The slowest transit time was observed during the morphine phase, which was significantly different from morphine with NX3G and placebo. The pain perception was not significantly influenced by NX3G. Conclusions, Orally administered NX3G is able to reverse the morphine-induced delay of CTT in humans without being detected in peripheral blood samples. Therefore, NX3G may improve symptoms of constipation in-patients using opioid medication without affecting opioid-analgesic effects. [source] Non-prostanoid prostacyclin mimetics as neuronal stimulants in the rat: comparison of vagus nerve and NANC innervation of the colonBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2000John A Rudd The spontaneous activity of the rat isolated colon is suppressed by prostacyclin analogues such as cicaprost (IC50=4.0 nM). Activation of prostanoid IP1 -receptors located on NANC inhibitory neurones is involved. However, several non-prostanoids, which show medium to high IP1 agonist potency on platelet and vascular preparations, exhibit very weak inhibitory activity on the colon. The aim of the study was to investigate this discrepancy. Firstly, we have demonstrated the very high depolarizing potency of cicaprost on the rat isolated vagus nerve (EC50=0.23 nM). Iloprost, taprostene and carbacyclin were 7.9, 66, and 81 fold less potent than cicaprost, indicating the presence of IP1 as opposed to IP2 -receptors. Three non-prostanoid prostacyclin mimetics, BMY 45778, BMY 42393 and ONO-1301, although much less potent than cicaprost (195, 990 and 1660 fold respectively), behaved as full agonists on the vagus nerve. On re-investigating the rat colon, we found that BMY 45778 (0.1,3 ,M), BMY 42393 (3 ,M) and ONO-1301 (3 ,M) behaved as specific IP1 partial agonists, but their actions required 30,60 min to reach steady-state and only slowly reversed on washing. This profile contrasted sharply with the rapid and readily reversible contractions elicited by a related non-prostanoid ONO-AP-324, which is an EP3 -receptor agonist. The full versus partial agonism of the non-prostanoid prostacyclin mimetics may be explained by the markedly different IP1 agonist sensitivities of the two rat neuronal preparations. However, the slow kinetics of the non-prostanoids on the NANC system of the colon remain unexplained, and must be taken into account when characterizing neuronal IP-receptors. British Journal of Pharmacology (2000) 129, 782,790; doi:10.1038/sj.bjp.0703090 [source] Escherichia coli,-haemolysin induces focal leaks in colonic epithelium: a novel mechanism of bacterial translocationCELLULAR MICROBIOLOGY, Issue 10 2007Hanno Troeger Summary Extraintestinal pathogenic Escherichia coli (ExPEC) are usually harmless colonizer of the intestinal microflora. However, they are capable to translocate and cause life-threatening disease. Translocation of ExPEC isolates was quantified in colonic monolayers. Transepithelial resistance (Rt) was monitored and local changes in conductivity analysed with conductance scanning. Confocal microscopy visualized the translocation route. Corroboratory experiments were performed on native rat colon. One translocating strain E. coli O4 was identified. This translocation process was associated with an Rt decrease (36 ± 1% of initial resistance) beginning only 2 h after inoculation. The sites of translocation were small defects in epithelial integrity (focal leaks) exhibiting highly increased local ion permeability. Translocation was enhanced by preincubation of monolayers with tumour necrosis factor-, or interleukin-13. Mutant strains lacking alpha-haemolysin lost the ability to induce focal leaks, while this effect could be restored by re-introducing the haemolysin determinant. Filtrate of a laboratory strain carrying the alpha-haemolysin operon was sufficient for focal leak induction. In native rat colon, E. coli O4 decreased Rt and immunohistology demonstrated focal leaks resembling those in cell monolayers. E. coli,-haemolysin is able to induce focal leaks in colonic cell cultures as well as in native colon. This process represents a novel route of bacterial translocation facilitated by pro-inflammatory cytokines. [source] Endogenous endothelin in a rat model of acute colonic mucosal injuryJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2000Masamitsu Sugimachi Abstract Background: Endothelin (ET) is involved in various biologic activities in non-vascular and vascular tissues. While ET has some significant effects on gastrointestinal functions, the possible role of endogenous ET in the host response to mucosal injury has not been well clarified. Methods: The present study describes an investigation of the effects of an endothelin A receptor antagonist, BQ-123, on lactate dehydrogenase (LDH), mucus and albumin flux into the perfusate in a rat model of acute colonic injury, induced by acetic acid perfusion. The present study also examined localization of ET in damaged rat colons by using immunohistochemistry. Results: A 4% acetic acid treatment induced mild mucosal damage of perfused rat colon and increased LDH as well as albumin and protein-bound hexose release into the perfusate. Pretreatment with BQ-123 significantly reduced LDH activity and protein-bound hexose concentration in the perfusate and delayed the reduction of albumin leakage from damaged mucosa. Vascular endothelial, neural and surface epithelial cells of the colon showed strong ET-like immunoreactivity. Mucosal damage markedly influenced ET expression by epithelial cells. Mild mucosal damage decreased the ET expression by surface epithelial cells while moderate mucosal damage induced a mosaic location of ET-positive epithelial cells in the crypt. Severe mucosal damage abolished the ET expression by epithelial cells. Conclusions: Endothelin may play a role in the host response to acute mucosal damage. Mucosal ET production is significantly affected by mucosal injury. [source] | |||||||||||||