Inhibition of p38 MAPK improves intestinal disturbances and oxidative stress induced in a rabbit endotoxemia model

Gonzálo, Sergio; Grasa, Laura; Arruebo, M. P.; Plaza, Miguel Ángel; Murillo, María Divina

doi:10.1111/j.1365-2982.2009.01439.x

Cited by 23 publications

(32 citation statements)

References 49 publications

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“…In this study we demonstrate that blockade of p38, JNK1/2 or ERK1/2 pathways abolished the effect of LPS on the acetylcholine-induced contractions in rabbit ileum. We have shown similar results in rabbit duodenum (6,8,9) although there are some differences. The effect of LPS in the longitudinal layer is higher in the duodenum than in the ileum (58 vs. 43% of reduction), while the effect of LPS is similar in the circular layer of duodenum and ileum.…”

Section: Discussionsupporting

confidence: 74%

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Mitogen activated protein kinases blockade improves lipopolysaccharide-induced ileal motor disturbances

Gonzálo

Grasa

Hernández

et al. 2012

Rev. esp. enferm. dig.

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Background: several diseases such as sepsis can affect the ileum. Lipopolysaccharide (LPS), an endotoxin present in the cell wall of gram negative bacteria, is a causative agent of sepsis.Objectives: the aims of this study were: a) to investigate the role of mitogen activated protein kinases (MAPKs) in the effect of LPS on the acetylcholine-induced contractions of rabbit ileum; and b) to study the localization of MAPKs in the ileum.Material and methods: ileal contractility was studied in an organ bath and MAPKs were localized by immunohistochemistry.Results: acetylcholine-induced contractions decreased with LPS. SB203580, SP600125 and U0126 blocked the effect of LPS on the acetylcholine-induced contractions. Phosphorylated p38 and ERK were detected in neurons of myenteric plexus and phosphorylated p38 and JNK in smooth muscle cells of ileum.Conclusion: we can suggest that p38, JNK, and ERK MAPKs are involved in the mechanism of action of LPS in the ileum. INTRODUCTIONGastrointestinal stasis is a common complication of sepsis (1,2). Lipopolysaccharide (LPS), an endotoxin present in the cell wall of gram negative bacteria, is widely used to reproduce sepsis symptoms. For example, LPS administration results in a decrease in contractility of ileal longitudinal smooth muscle (3).Mitogen activated protein kinases (MAPKs) are a family of protein kinases involved in many cellular programs such as cell proliferation, cell differentiation and cell death and it has been observed an abnormal activation of MAPKs in pathological circumstances such as sepsis. The most important groups of MAPKs are the p38, c-Jun-N-terminal kinase (JNK1/2) and extracellular signal-regulated kinase (ERK1/2) MAPK(4).The aims of this study were: (1) to investigate the role of MAPKs in the effect of LPS on the acetylcholine-induced contractions of rabbit ileum and (2) to study the localization of MAPKs in the ileum. MATERIALS AND METHODS Drugs and solutions Acetylcholine (ACh) and lipopolysaccharide (LPS, from AnimalsAll experimental protocols were approved by the Ethics Committee of the University of Zaragoza (Spain). Male New Zealand rabbits weighing 2-2.25 kg were kept with standard rabbit fodder and free access to water. Vol. 104. N.° 6, pp. 305-309, 2012 This work was presented, in part, at the "LXVII Congreso Mitogen activated protein kinases blockade improves lipopolysaccharide-induced ileal motor disturbances

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Section: Discussionsupporting

confidence: 74%

“…In previous studies we have described a similar localization of these MAPKs in the rabbit duodenum, although the expression of p-p38 and p-ERK1/2 in the smooth muscle of duodenum was lower than in ileum (6,8,9).…”

Section: Discussionmentioning

confidence: 91%

Mitogen activated protein kinases blockade improves lipopolysaccharide-induced ileal motor disturbances

Gonzálo

Grasa

Hernández

et al. 2012

Rev. esp. enferm. dig.

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“…Previous studies have reported high expression of phospho-p38 MAPK in neurons of rabbit duodenum (GONZALO et al, 2010). Also, it has been showed that surgical manipulation can lead to oxidative stress (ANUP et al, 1999).…”

Section: Resultsmentioning

confidence: 99%

Topical and intraluminal Carolina Rinse Solution in p44/42 and p38 MAP Kinase activation profile in rabbit jejunum after ischemia and reperfusion

et al. 2013

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The effects of topical and intraluminal Carolina Rinse Solution (CRS) in p44/42 (ERK 1/2) and p38 MAPK activation profi le, in rabbit jejunum after ischemia and reperfusion (I/R), were investigated in this study. Fifteen New Zealand rabbits were allocated in three groups: Sham-operated (A), Ischemia and reperfusion (B) and CRS (C). Groups B and RESUMO Os efeitos do uso tópico e intraluminal da Solução de Carolina Rinse (CRS), no perfi l de ativação das MAP quinases p44/42 (ERK 1/2) e p38, no jejuno de coelhos após isquemia e reperfusão (I/R), foram investigados neste estudo. Quinze coelhos da raça Nova Zelândia foram alocados em três grupos: Instrumentado (A), Isquemia e Reperfusão (B) e CRS (C). Os grupos B e C foram submetidos a uma hora de isquemia

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“…COX-2 is an inducible form of the enzyme produced in a variety of stress conditions, such as sepsis 4 , tumor 5 , operative manipulation 6 and bowel obstruction 7 . Recent studies indicate that inducible expression of COX-2 in endotoxemia rats induces the motility disturbance of intestine 8,9 . Conversely, suppression of COX-2 using inhibitor of mitogen activated protein kinase attenuates the intestinal dysmotility 8,9 .…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies indicate that inducible expression of COX-2 in endotoxemia rats induces the motility disturbance of intestine 8,9 . Conversely, suppression of COX-2 using inhibitor of mitogen activated protein kinase attenuates the intestinal dysmotility 8,9 . These findings suggest that COX-2 is associated with the development of the intestinal dysmotility induced by endotoxin.…”

Section: Introductionmentioning

confidence: 99%

Enhanced cyclooxygenase-2 activity leads to intestinal dysmotility following hemorrhagic shock

et al. 2015

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PURPOSE:To test whether hemorrhagic shock (HS) increases the Cyclooxygenase-2 (COX-2) expression in the intestine and whether this enhanced COX-2 expression mediates the intestinal dysmotility after HS. METHODS: Male Wistar rats were randomly divided into HS sham group and HS group. At 180 min following HS establishment, the duodenum samples were harvested to assess the motility function, protein expression of COX-2 and the downstream products of COX-2, prostaglandins . RESULTS: Examination of motility function ex vivo showed that the contractile response to acetylcholine of smooth muscle strips of rats subjected to HS was significantly suppressed. A COX-2 inhibitor, NS-398, abolished this depressed contractile response after HS. Western blotting revealed an increased protein expression of COX-2 in intestinal tissues of HS rats. Immunohistochemical examination indicated that intestine tissues of HS rats were manifested by part of villous expansion and disruption, a large amount of COX-2 positive cells appearance in lamina propria and submucosa. Furthermore, the contents of prostaglandin E 2 was significantly increased in intestinal tissues of HS rats. CONCLUSION: The enhanced COX-2/ prostaglandin E 2 involves in the hemorrhagic shock induced intestinal dysmotility.

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Inhibition of p38 MAPK improves intestinal disturbances and oxidative stress induced in a rabbit endotoxemia model

Abstract: Lipopolysaccharide decreases the duodenal contractility in rabbits and increases the production of free radicals. p38 MAPK is a mediator of these effects.

Cited by 23 publications

References 49 publications

Mitogen activated protein kinases blockade improves lipopolysaccharide-induced ileal motor disturbances

Mitogen activated protein kinases blockade improves lipopolysaccharide-induced ileal motor disturbances

Topical and intraluminal Carolina Rinse Solution in p44/42 and p38 MAP Kinase activation profile in rabbit jejunum after ischemia and reperfusion

Enhanced cyclooxygenase-2 activity leads to intestinal dysmotility following hemorrhagic shock

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