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L P Filaretova - One of the best experts on this subject based on the ideXlab platform.
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somatic pain sensitivity under indometacin induced Gastric and small intestinal injury in rats
Fiziologicheskiĭ zhurnal, 2014Co-Authors: N I Iarushkina, T R Bagaeva, L P FilaretovaAbstract:The aim was to study the effect of indometacin (IM) induced gastrointestinal injury on somatic pain sensitivity in awake rats. IM was administered at the ulcerogenic dose (35 mg/kg, s. c.) to fasted (24 h) and fed rats. Somatic pain sensitivity was evaluated using a tail flick test. Latency time was measured under conditions of the formation of Gastric Erosion (1 - 4 h after IM injection) as well as small intestinal injury (24, 48 and 72 h after IM injection). IM administration caused the Gastric Erosion formation only in fasted rats (4 h after the administration) and the small intestinal injury in both fasted and fed rats (24, 48, 72 h after the administration). Indomethacin-caused Gastric and small intestinal injury resulted in an increase in tail flick latency. We did not observe any changes in tail flick latency in IM-treated rats without significant gastrointestinal injury. The gastrointestinal injury was accompanied by signs of chronic stress: long-lasting increase in corticosterone blood level, adrenal hypertrophy, thymus involution, and loss of body weight. Thus, the IM-induced gastrointestinal injury formation resulted in somatic pain inhibition in awake rats.
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A wider view on Gastric Erosion: Detailed evaluation of complex somatic and behavioral changes in rats treated with indomethacin at Gastric ulcerogenic dose
Endocrine regulations, 2014Co-Authors: L P Filaretova, T R Bagaeva, O. Morozova, Dóra ZelenaAbstract:Objective. Gastric Erosion is widespread side effect of nonsteroidal anti-inflammatory drugs. To examine the complexity of the brain-gut axis regulation, indomethacin-induced Gastric Erosion formation was studied in connection with somatic and behavioral changes.Methods. During a constant telemetric recording of heart rate, body temperature, and locomotion of male rats we examined the effects of 24 h fasting, indomethacin (35 mg/kg s.c.) injection, and refeeding at 4 h. Behavior was analyzed on elevated plus maze (EPM) at 24 h and somatic changes at 72 h.Results. Gastric Erosion developed 4 h after indomethacin injection, healed 72 h later contrasted by large injury in the small intestine. As classical signs of chronic stress, body and thymus weight were reduced while adrenal weight was enhanced 72 h after indomethacin injection. Fasting by itself changed all telemetrically recorded parameters with most prominent decrease in heart rate. Indomethacin induced similar diminishing effects with earliest and strongest temperature decrease. As a sign of more anxious phenotype locomotion reducing effect of indomethacin injection was detected on EPM. The EPM-induced temperature elevation was missing in indomethacin-treated animals.Conclusions. Fasting by itself induce somatic changes, which can make the animals more vulnerable to ulcerogenic stimuli. Development of indomethacin-induced gastrointestinal lesions happened in parallel with disturbances of heart rate, core body temperature, and chronic stress-like somatic changes as well as anxiety-like behavior. We have to be more aware of the existence of the brain-gut axis and should study changes in the whole body rather than focusing on a specific organ. KEYWORDS: indomethacin, gastrointestinal injury, telemetry, heart rate, body temperature, locomotion, somatic parameters, elevated plus maze.
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A comparative analysis of corticosterone, cortisol and dexametasone effects on Gastric Erosion in rats
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2012Co-Authors: T R Bagaeva, Morozova Oiu, L P FilaretovaAbstract:We previously demonstrated that manifestation of gastroprotective or proulcerogenic effects of single dexamethasone injection depends on duration of the hormonal action before ulcerogenic stimulus, but not on the hormonal dose. In the present study we investigated dose and time dependence of corticosterone and cortisol effects on the Gastric Erosion in rats in comparative aspect with dexamethasone effects. Gastric Erosion was induced by indomethacin (35 mg/kg, sc) in preliminary fasted rats. Single injection of corticosterone or cortisol at the doses of 25, 50, 100 mg/kg one hour before indomethacin administration resulted in dose dependent gastroprotective effects similar to dexamethasone effects. However, after extending the hormonal action till 24 h (before indomethacin administration), the gastroprotective effect of corticosterone (100 mg/kg) and cortisol (50 mg/kg) didn't transform into a proulcerogenic one, in contrast to dexamethasone, but simply disappeared. The absence of long-lasting corticosterone deficiency in blood after corticosterone and cortisol injection, which was observed after dexamethasone injection, could be at least one of the possible reasons for the absence of transformation of the gastroprotective action of corticosterone and cortisol to a proulcerogenic one.
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Dual action of glucocorticoid hormones on the Gastric mucosa: how the gastroprotective action can be transformed to the ulcerogenic one
Inflammopharmacology, 2009Co-Authors: L P Filaretova, T R Bagaeva, T. T. Podvigina, O. MorozovaAbstract:Glucocorticoid hormones have dual action on the stomach: gastroprotective and ulcerogenic one. The present study was designed to investigate how physiological gastroprotective action of glucocorticoids can be transformed to pathological ulcerogenic effect. Dose- and time-dependent effects of single injection of dexamethasone on indomethacin-induced Gastric Erosions, corticosterone and blood glucose levels, somatic parameters were investigated in rats. Dexamethasone at the doses of 0.1, 1, 10 mg/kg decreased the Gastric Erosion area dose dependently in the case of its injection 1 h before indomethacin administration. Gastroprotective action of dexamethasone (at a dose of 1 mg/kg) was also observed in the case of its injection 6 and 12 h before indomethacin. However, the further increase in the time interval caused transformation of gastroprotective action of dexamethasone to ulcerogenic one. Accordingly to the data obtained short-term maintenance of blood glucose level provides the gastroprotective action of dexamethasone, while dexamethasone-induced long-lasting maintenance of blood glucose level accompanied with the signs of catabolic effects may be responsible at least partly for its ulcerogenic effect.
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Contribution of glucocorticoids to protective influence of preconditioning mild stress against stress-induced Gastric Erosions.
Annals of the New York Academy of Sciences, 2008Co-Authors: L P Filaretova, T R Bagaeva, Kikuko Amagase, Koji TakeuchiAbstract:It is known that preconditioning stress may attenuate stress-induced Gastric injury and that this effect is mediated by prostaglandins. In the present study we investigated the contribution of glucocorticoids to the gastroprotective effect of preconditioning stress. The effects of mild stress on Gastric Erosion caused by severe stress were compared in rats with normal and deficient corticosterone response to preconditioning mild stress. Mild stress decreased the Gastric ulceration caused by severe stress, and this effect was prevented by glucocorticoid deficiency during mild stress. The results suggest that glucocorticoids released during preconditioning mild stress contribute to the gastroprotective effect of this stress.
Gergely Klausz - One of the best experts on this subject based on the ideXlab platform.
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polymorphisms of the apoe hsd3b1 il 1β and p53 genes are associated with the development of early uremic complications in diabetic patients results of a dna resequencing array study
International Journal of Molecular Medicine, 1998Co-Authors: Dominika Szoke, Bela Molnar, Norbert Solymosi, Karoly Racz, Peter Gergics, Bernadett Blasko, Barna Vasarhelyi, Adam Vannay, Y Mandy, Gergely KlauszAbstract:: Genetic polymorphisms of the genes involved in angiogenesis, the inflammatory cascade or apoptosis control can influence the chronic complications of diabetic patients. Parallel evaluation of multiple genetic polymorphisms became available with the development of DNA resequencing arrays. We aimed to develop a 16-gene, 18,859-nucleotide resequencing array to analyze the genetic background of uremic and gastrointestinal complications. DNA was isolated from 10 ml of peripheral blood of 41 non-uremic and 37 uremic patients with type II diabetes mellitus (DM); 32 suffering from Gastric Erosion complications. An Affymetrix Customseq Resequencing array was developed containing a total of 37 PCR products of selected genes. Confirmatory analysis was performed for 5 known polymorphisms by RFLP and for 4 others by capillary sequencing. Statistical analysis was performed using the Fisher's exact test. Correlations between the DNA resequencing array and the confirmatory methods were 96% for RFLP and 99.4% for capillary sequencing. The genetic polymorphisms of the ApoE, HSD3B1, IL-1beta and p53 genes were found to be significantly different (p<0.05) between the uremic and non-uremic diabetes group. In regards to the Gastric Erosion complications of the diabetic uremic patients, the A17708T polymorphism of the p53 intron 10 was found to have a statistically significant (p<0.05) role. In conclusion, DNA sequencing arrays can contribute to a multiparameter genetic analysis yielding highly correlating results using a single method in patients suffering type II DM.
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Polymorphisms of the ApoE, HSD3B1, IL-1β and p53 genes are associated with the development of early uremic complications in diabetic patients: Results of a DNA resequencing array study
International Journal of Molecular Medicine, 1998Co-Authors: Dominika Szoke, Bela Molnar, Norbert Solymosi, Karoly Racz, Peter Gergics, Bernadett Blasko, Barna Vasarhelyi, Adam Vannay, Y Mandy, Gergely KlauszAbstract:Genetic polymorphisms of the genes involved in angiogenesis, the inflammatory cascade or apoptosis control can influence the chronic complications of diabetic patients. Parallel evaluation of multiple genetic polymorphisms became available with the development of DNA resequencing arrays. We aimed to develop a 16-gene, 18,859-nucleotide resequencing array to analyze the genetic background of uremic and gastrointestinal complications. DNA was isolated from 10 ml of peripheral blood of 41 non-uremic and 37 uremic patients with type II diabetes mellitus (DM); 32 suffering from Gastric Erosion complications. An Affymetrix Customseq Resequencing array was developed containing a total of 37 PCR products of selected genes. Confirmatory analysis was performed for 5 known polymorphisms by RFLP and for 4 others by capillary sequencing. Statistical analysis was performed using the Fisher's exact test. Correlations between the DNA resequencing array and the confirmatory methods were 96% for RFLP and 99.4% for capillary sequencing. The genetic polymorphisms of the ApoE, HSD3B1, IL-1beta and p53 genes were found to be significantly different (p
Radu Pescarus - One of the best experts on this subject based on the ideXlab platform.
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Case Report: Endoscopic Removal of an Eroded Gastric Band Causing Small Bowel Obstruction upon Migration into the Proximal Jejunum
Obesity Surgery, 2020Co-Authors: Amir Sleiman, Anne Sophie Studer, Pierre Y. Garneau, Ronald Denis, Mark Magdy, Majed Alanazi, Radu PescarusAbstract:Background Adjustable Gastric banding (AGB) is on the decline due to its relatively modest amount of expected weight loss, coupled with high rates of revision and complications such as band Erosion. Management of eroded Gastric bands can be challenging especially when complete intra-Gastric Erosion is followed by distal migration causing small bowel obstruction. Methods We present an endoscopic option of using a pediatric colonoscope to remove an eroded AGB causing jejunal obstruction. Result Endoscopic removal of an eroded ABG causing bowel obstruction was successful. Conclusion Endoscopy remains a safe and relatively non-invasive approach to deal with such complications.
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Case Report: Endoscopic Removal of an Eroded Gastric Band Causing Small Bowel Obstruction upon Migration into the Proximal Jejunum
Obesity Surgery, 2020Co-Authors: Amir Sleiman, Anne Sophie Studer, Pierre Y. Garneau, Ronald Denis, Mark Magdy, Majed Alanazi, Radu PescarusAbstract:Background Adjustable Gastric banding (AGB) is on the decline due to its relatively modest amount of expected weight loss, coupled with high rates of revision and complications such as band Erosion. Management of eroded Gastric bands can be challenging especially when complete intra-Gastric Erosion is followed by distal migration causing small bowel obstruction. Methods We present an endoscopic option of using a pediatric colonoscope to remove an eroded AGB causing jejunal obstruction. Result Endoscopic removal of an eroded ABG causing bowel obstruction was successful. Conclusion Endoscopy remains a safe and relatively non-invasive approach to deal with such complications.
T R Bagaeva - One of the best experts on this subject based on the ideXlab platform.
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somatic pain sensitivity under indometacin induced Gastric and small intestinal injury in rats
Fiziologicheskiĭ zhurnal, 2014Co-Authors: N I Iarushkina, T R Bagaeva, L P FilaretovaAbstract:The aim was to study the effect of indometacin (IM) induced gastrointestinal injury on somatic pain sensitivity in awake rats. IM was administered at the ulcerogenic dose (35 mg/kg, s. c.) to fasted (24 h) and fed rats. Somatic pain sensitivity was evaluated using a tail flick test. Latency time was measured under conditions of the formation of Gastric Erosion (1 - 4 h after IM injection) as well as small intestinal injury (24, 48 and 72 h after IM injection). IM administration caused the Gastric Erosion formation only in fasted rats (4 h after the administration) and the small intestinal injury in both fasted and fed rats (24, 48, 72 h after the administration). Indomethacin-caused Gastric and small intestinal injury resulted in an increase in tail flick latency. We did not observe any changes in tail flick latency in IM-treated rats without significant gastrointestinal injury. The gastrointestinal injury was accompanied by signs of chronic stress: long-lasting increase in corticosterone blood level, adrenal hypertrophy, thymus involution, and loss of body weight. Thus, the IM-induced gastrointestinal injury formation resulted in somatic pain inhibition in awake rats.
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A wider view on Gastric Erosion: Detailed evaluation of complex somatic and behavioral changes in rats treated with indomethacin at Gastric ulcerogenic dose
Endocrine regulations, 2014Co-Authors: L P Filaretova, T R Bagaeva, O. Morozova, Dóra ZelenaAbstract:Objective. Gastric Erosion is widespread side effect of nonsteroidal anti-inflammatory drugs. To examine the complexity of the brain-gut axis regulation, indomethacin-induced Gastric Erosion formation was studied in connection with somatic and behavioral changes.Methods. During a constant telemetric recording of heart rate, body temperature, and locomotion of male rats we examined the effects of 24 h fasting, indomethacin (35 mg/kg s.c.) injection, and refeeding at 4 h. Behavior was analyzed on elevated plus maze (EPM) at 24 h and somatic changes at 72 h.Results. Gastric Erosion developed 4 h after indomethacin injection, healed 72 h later contrasted by large injury in the small intestine. As classical signs of chronic stress, body and thymus weight were reduced while adrenal weight was enhanced 72 h after indomethacin injection. Fasting by itself changed all telemetrically recorded parameters with most prominent decrease in heart rate. Indomethacin induced similar diminishing effects with earliest and strongest temperature decrease. As a sign of more anxious phenotype locomotion reducing effect of indomethacin injection was detected on EPM. The EPM-induced temperature elevation was missing in indomethacin-treated animals.Conclusions. Fasting by itself induce somatic changes, which can make the animals more vulnerable to ulcerogenic stimuli. Development of indomethacin-induced gastrointestinal lesions happened in parallel with disturbances of heart rate, core body temperature, and chronic stress-like somatic changes as well as anxiety-like behavior. We have to be more aware of the existence of the brain-gut axis and should study changes in the whole body rather than focusing on a specific organ. KEYWORDS: indomethacin, gastrointestinal injury, telemetry, heart rate, body temperature, locomotion, somatic parameters, elevated plus maze.
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A comparative analysis of corticosterone, cortisol and dexametasone effects on Gastric Erosion in rats
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2012Co-Authors: T R Bagaeva, Morozova Oiu, L P FilaretovaAbstract:We previously demonstrated that manifestation of gastroprotective or proulcerogenic effects of single dexamethasone injection depends on duration of the hormonal action before ulcerogenic stimulus, but not on the hormonal dose. In the present study we investigated dose and time dependence of corticosterone and cortisol effects on the Gastric Erosion in rats in comparative aspect with dexamethasone effects. Gastric Erosion was induced by indomethacin (35 mg/kg, sc) in preliminary fasted rats. Single injection of corticosterone or cortisol at the doses of 25, 50, 100 mg/kg one hour before indomethacin administration resulted in dose dependent gastroprotective effects similar to dexamethasone effects. However, after extending the hormonal action till 24 h (before indomethacin administration), the gastroprotective effect of corticosterone (100 mg/kg) and cortisol (50 mg/kg) didn't transform into a proulcerogenic one, in contrast to dexamethasone, but simply disappeared. The absence of long-lasting corticosterone deficiency in blood after corticosterone and cortisol injection, which was observed after dexamethasone injection, could be at least one of the possible reasons for the absence of transformation of the gastroprotective action of corticosterone and cortisol to a proulcerogenic one.
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Dual action of glucocorticoid hormones on the Gastric mucosa: how the gastroprotective action can be transformed to the ulcerogenic one
Inflammopharmacology, 2009Co-Authors: L P Filaretova, T R Bagaeva, T. T. Podvigina, O. MorozovaAbstract:Glucocorticoid hormones have dual action on the stomach: gastroprotective and ulcerogenic one. The present study was designed to investigate how physiological gastroprotective action of glucocorticoids can be transformed to pathological ulcerogenic effect. Dose- and time-dependent effects of single injection of dexamethasone on indomethacin-induced Gastric Erosions, corticosterone and blood glucose levels, somatic parameters were investigated in rats. Dexamethasone at the doses of 0.1, 1, 10 mg/kg decreased the Gastric Erosion area dose dependently in the case of its injection 1 h before indomethacin administration. Gastroprotective action of dexamethasone (at a dose of 1 mg/kg) was also observed in the case of its injection 6 and 12 h before indomethacin. However, the further increase in the time interval caused transformation of gastroprotective action of dexamethasone to ulcerogenic one. Accordingly to the data obtained short-term maintenance of blood glucose level provides the gastroprotective action of dexamethasone, while dexamethasone-induced long-lasting maintenance of blood glucose level accompanied with the signs of catabolic effects may be responsible at least partly for its ulcerogenic effect.
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Effect of dexamethasone on indomethacin-induced Gastric Erosion formation upon duration of the hormonal action
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2009Co-Authors: Morozova Oiu, T R BagaevaAbstract:The aim of the study was to verify a dependence of dexamethasone effect on the Gastric Erosion formation upon duration of the hormonal action. Gastric Erosions were induced by indometha cin (35 mg/kg, sc) in male rats after 24-hour fasting. The rats were given a single injection of dexamethasone at a dose of 1 mg/kg and they underwent the ulcerogenic stimulus (indomethacin) at va rious time points after the hormonal injection (1, 6, 12, 18, 24 hours as well as 3, 5, 7 days). The control rats were given dexamethasone vehicle. In 4 hours after indomethacin injection Gastric Erosions, corticosterone and blood glucose levels, as well as body and thymus weights were examined. The results obtained demonstrate a dependence ofdexamethasone effect on the Gastric Erosion formation upon duration of its action: dexamethasone attenuated or aggravated indomethacin-induced Gastric Erosions depending on the time of its injection. Gastroprotective action of dexamethasone was observed in the case of its injection 1, 6, and 12 hours before indomethacin. The further increase in the time interval caused transformation of gastroprotective action of dexamethasone against ulcerogenic effect. The data obtained suggest that a disturbance of carbohydrate regulation accompanied with the signs of catabolic effects of the glucocorticoid may be responsible for the ulcerogenic action of dexamethasone.
Hiroshi Demura - One of the best experts on this subject based on the ideXlab platform.
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Interleukin-1 inhibits stress-induced Gastric Erosion in rats.
Life sciences, 1991Co-Authors: Tamotsu Shibasaki, Naoko Yamauchi, Mari Hotta, Toshihiro Imaki, Toshihiko Oda, Nicholas Ling, Hiroshi DemuraAbstract:Abstract The effect of interleukin (IL)-1 on the occurence of stress-induced Gastric Erosions was examined in rats. The intracerebroventricular (icv) administration of IL-1β significantly inhibited the occurence of water-immersion restraint stress-induced Gastric Erosion at doses of 200 ng, 500 ng and 1 μg, whereas the intravenous (iv) administration of IL-1β altered the occurence of Gastric Erosion only at a dose of 1 μg. The inhibitory effect of IL-1α icv administered on the occurence of Gastric Erosion was found only at a dose of 1 μg. The inhibitory effect of IL-1β icv administered on the occurence of stress-induced Gastric Erosion was not influenced by icv administration of α-helical CRF(9–41), a corticotropin-releasing factor (CRF) receptor antagonist. Indomethacin completely blocked the inhibitory action of IL-1β icv administered on stress-induced Gastric Erosion. It is concluded from these results that IL-1 acts mainly in the central nervous system to inhibit the occurence of stress-induced Gastric Erosion and that the IL-1β-induced inhibition of Gastric Erosion is mediated by prostaglandin in a manner that is independent of brain CRF.