Endothelin-3 induced mesenteric vasoconstriction and PMN infiltration in the rat small intestine: role of endothelin receptors

Ghandour, Salah; Çetınel, Şule; Kurtel, Hızır

doi:10.1016/j.regpep.2004.01.007

Cited by 5 publications

(6 citation statements)

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“…Intestinal ischemia-reperfusion results in organ injury through both tissue hypoxia and reperfusion phenomena mediated by inflammatory response and oxidative stress [9,10] . There is increasing evidence that the inflammatory response and oxidative stress in the small intestine exert important roles in the bacteria or endotoxin translocation and the development of SIRS after thermal injury [11][12][13][14][15] . Evidence has indicated that endogenous carbon monoxide (CO), a biproduct of inducible heme oxygenase can modulates inflammation.…”

Section: Introductionmentioning

confidence: 99%

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Liu

Sun

et al. 2008

Acta Pharmacologica Sinica

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Aim: To determine whether carbon monoxide (CO)-releasing molecules-liberated CO suppress inflammatory cytokine production and oxidative stress in the small intestine of burnt mice. Methods: Twenty-eight mice were assigned to 4 groups. The mice in the sham group (n=7) underwent sham thermal injury, whereas the mice in the burn group (n=7) received 15% total body surface area full-thickness thermal injury, the mice in the burn+CO-releasing molecules (CORM)-2 group (n=7) underwent the same injury with immediate administration of CORM-2 (8 mg/kg, iv), and the mice in the burn+inactivated CORM (iCORM)-2 group (n=7) underwent the same injury with immediate administration of iCORM-2. The levels of inflammatory cytokines in the tissue homogenates were measured by ELISA. The levels of malondialdehyde (MDA), nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) in the small intestine were also assessed. In the in vitro experiment, Caco-2 cells were stimulated by experimental mouse sera (50%, v/v) for 4 h. Subsequently, the levels of interleukin (IL)-8 and NO in the supernatants were assessed. Reactive oxygen species (ROS) generation in Caco-2 cells was also measured. Results: The treatment of burnt mice with CORM-2 significantly attenuated the levels of IL-1β, TNF-α, MDA, and NO in tissue homogenates. This was accompanied by a decrease of iNOS expression. In parallel, the levels of IL-8, NO, and intracellular ROS generation in the supernatants of Caco-2 stimulated by the CORM-2-treated burnt mouse sera was markedly decreased. Conclusion: CORM-released CO attenuates the production of inflammatory cytokines, prevents burn-induced ROS generation, and suppresses the oxidative stress in the small intestine of burnt mice by interfering with the protein expression of iNOS.

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Section: Introductionmentioning

confidence: 99%

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Liu

Sun

et al. 2008

Acta Pharmacologica Sinica

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“…A variety of cytokines are released into the microcirculation by neutrophils, endothelial cells and monocytes during phases of hypoxia and reperfusion [7,8] . Although the pathophysiological basis of organ damage remains unclear, there is increasing evidence that leukocyte infiltration into intestinal tissue plays an important role in bacterial or endotoxin translocation and development of SIRS after thermal injury [9][10][11][12] . A lot of evidence indicates that endogenous Carbon (CO), a by-product of inducible heme oxygenase (HO-1) Abstract AIM: To determine whether Carbon (CO) liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice.…”

Section: Introductionmentioning

confidence: 99%

Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

Sun¹,

Jin²,

Sun³

et al. 2007

WJG

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INTRODUCTIONSystemic inflammator y response syndrome (SIRS) and multiple organ failure (MOF) still continue to be leading causes of morbidity and mortality in severe burn patients [1,2] . The intestine is considered to be the critical organ in the development of organ dysfunction in trauma, burns, and intensive care unit patients [3] . Thermal injury is accompanied by complex events that exert deleterious effects on various organs, such as the small intestine, distant from the original burn wound. Following thermal injury, the small intestine is subjected to ischemia, and consequently, especially during burn resuscitation, reperfusion injury occurs [4] . Intestinal ischemia-reperfusion results in organ injury through both tissue hypoxia and reperfusion phenomena mediated by neutrophils [5,6] . A variety of cytokines are released into the microcirculation by neutrophils, endothelial cells and monocytes during phases of hypoxia and reperfusion [7,8] . Although the pathophysiological basis of organ damage remains unclear, there is increasing evidence that leukocyte infiltration into intestinal tissue plays an important role in bacterial or endotoxin translocation and development of SIRS after thermal injury [9][10][11][12] . A lot of evidence indicates that endogenous Carbon (CO), a by-product of inducible heme oxygenase (HO-1) Abstract AIM: To determine whether Carbon (CO) liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice.METHODS: Thirty-six mice were assigned to four groups. Mice in the sham group (n = 9) were underwent to sham thermal injury; mice in the burn group (n = 9) received 15% total body surface area full-thickness thermal injury; mice in the burn + CORM-2 group (n = 9) were underwent to the same thermal injury with immediate administration of tricarbonyldichlororut henium (Ⅱ) dimer CORM-2 (8 mg/kg, i.v.); and mice in the burn+DMSO group (n = 9) were underwent to the same thermal injury with immediate administration of 160 μL bolus injection of 0.5% DMSO/saline. Histological alterations and granulocyte infiltration of the small intestine were assessed. Polymorphonuclear neutrophil (PMN) accumulation (myeloperoxidase assay) was assessed in mice mid-ileum. Activation of nuclear factor (NF)-κΒ, expression levels of intercellular adhesion molecule-1 (ICAM-1) and inducible heme oxygenase in mid-ileum were assessed. RESULTS:Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-κΒ in the small intestine. This was accompanied by a decrease in the expression of ICAM-1. In parallel, burn-induced granulocyte infiltration in midileum was markedly decreased in the burn mice treated with CORM-2.

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“…Small intestines are the major source of ET-3 production [15]. ET-3 decreases superior mesenteric artery (SMA) blood flow significantly and plays important roles in intestinal mucosal dysfunction and tissue PMN infiltration [16]. In the present study tissue endothelin levels were not assayed but in experimental strangulated small bowel obstructions, the release and concentration of ET-1 has been shown to increased in the venous blood of strangulated intestinal loop.…”

Section: Discussionmentioning

confidence: 78%

Untitled

et al. 2006

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Background: Ischemia is the most important factor compromises wound healing in colonic anastomosis. Mesenteric vessels are ligated at first while performing colonic resection and following anastomosis. Therefore blood supply of the related segments of colon temporarily interrupted and ischemia can easily occur. This study was carried out to explore whether Bosentan, an endothelinreceptor antagonist, can eliminate vasoconstruction, increase blood flow in the splanchnic area and anastomotic region and therefore possibly facilitate wound healing and prevent intra-abdominal adhesion formation.

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Endothelin-3 induced mesenteric vasoconstriction and PMN infiltration in the rat small intestine: role of endothelin receptors

Cited by 5 publications

References 35 publications

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

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Endothelin-3 induced mesenteric vasoconstriction and PMN infiltration in the rat small intestine: role of endothelin receptors

Cited by 5 publications

References 35 publications

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice1

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice1

Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

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Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹