Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Li, Li; Zhang, Yongmei; Qiao, Wei; Wang, Lin; Zhang, Jian‐Fu

doi:10.3748/wjg.v13.i6.874

Cited by 9 publications

(17 citation statements)

References 42 publications

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“…Following thermal injury, the small intestine is subjected to ischemia, and consequently, especially during burn resuscitation, reperfusion injury occurs [8] . 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] .…”

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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“…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] .…”

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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“…The PVN also regulates classical neurotransmitters such as ACh, NE, 5-HT. Additionally, the PVN controls the parasympathetic and sympathetic nervous systems and the three endocrine glands (thyroid, adrenal and gonad) [20,35] . The PVN is also involved in TNBSinduced colitis [19,22] .…”

Section: Discussionmentioning

confidence: 99%

“…Efferent vagal fibers innervating the gut originate from the DVC [19,20] . A literature review demonstrated that stimulating the PVN influenced the activity of vagal efferent fibers.…”

Section: Introductionmentioning

confidence: 99%

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

Zhang

Fei

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of glutamate microinjection into hypothalamic paraventricular nucleus (PVN) on ulcerative colitis (UC) in rats and to explore the relevant mechanisms. Methods: 2,4,6-Trinitrobenzenesulfonic acid (100 mg/kg in 50% ethanol) was instilled into the colon of adult male SD rats to induce UC. A colonic damage score (CDS) was used to indicate the severity of the colonic mucosal damage. The pathological changes in the colonic mucosa were evaluated using immunohistochemistry, Western blotting, biochemical analyses or ELISA. Ten minutes before UC induction, drugs were microinjected into the relevant nuclei in rat brain to produce chemical stimulation or chemical lesion.Results: Microinjection of glutamate (3, 6 and 12 µg) into the PVN dose-dependently decreased the CDS in UC rats. This protective effect was eliminated after kainic acid (0.3 µg) was microinjected into PVN or into the nucleus tractus solitarius (NTS) that caused chemical lesion of these nuclei. This protective effect was also prevented when the AVP-V 1 receptor antagonist DPVDAV (200 ng) was microinjected into the NTS. The discharge frequency of the vagus was markedly decreased following microinjection of glutamate into the PVN. Microinjection of glutamate into the PVN in UC rats significantly increased the cell proliferation and anti-oxidant levels, and decreased the apoptosis and Bax and caspase 3 expression levels and reduced the pro-inflammatory factors in the colonic mucosa. Conclusion: The activation of hypothalamic PVN exerts protective effects against UC, which is mediated by the NTS and vagus. The effects may be achieved via anti-oxidative, anti-apoptotic, and anti-inflammatory factors.

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Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Cited by 9 publications

References 42 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

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

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Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Cited by 9 publications

References 42 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

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

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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