Stress and the Stomach: Corticotropin-Releasing Factor May Protect the Gastric Mucosa in Stress Through Involvement of Glucocorticoids

Filaretova, Ludmila; Bagaeva, T. R.; Morozova, Olga

doi:10.1007/s10571-012-9800-z

Cited by 18 publications

(7 citation statements)

References 28 publications

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“…Taking into consideration this fact together with the facts that humoral pathway and systemic response are two main pathways for the transmitting the RIPC-induced protective signals ( Lim and Hausenloy, 2012 ) it is reasonable to propose a participation of glucocorticoids in realization of gastroprotective effect of RIPC. Our previous findings about gastroprotective role of glucocorticoids also allowed us to assume that glucocorticoids may contribute to gastroprotective effect of RIPC ( Filaretova et al, 1998 ; Filaretova et al, 2004 ; Filaretova et al, 2007 ; Filaretova et al, 2008 , Filaretova et al, 2012 ; Filaretova, 2011 ; Filaretova, 2017 ; Filaretova and Bagaeva, 2016 ). Additionally it is important to note that we previously demonstrated participation of glucocorticoids in protective effect of local gastric ischemic preconditioning against I/R-induced gastric injury ( Bobryshev et al, 2009 ).…”

Section: Introductionmentioning

confidence: 84%

“…It was not assumed before to verify the participation of glucocorticoids in gastroprotective effect of RIPS, apparently due to the prevailing traditional point of view on ulcerogenic action of glucocorticoids released during stress. Nevertheless, our previous findings suggest that glucocorticoids released during acute stress-induced activation of the hypothalamic-pituitary-adrenocortical (HPA) axis are naturally occurring protective factors that play an important role in maintenance of the gastric mucosal integrity ( Filaretova et al, 1998 ; Filaretova et al, 2012 ; Filaretova 2011 ; Filaretova and Bagaeva 2016 ). It was demonstrated that glucocorticoids released during preconditioning mild stress contribute to the protective effect of this stress on gastric mucosa against cold-restraint-induced gastric lesions ( Filaretova et al, 2008 ; Filaretova, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

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Non-Invasive Remote Ischemic Preconditioning May Protect the Gastric Mucosa Against Ischemia-Reperfusion-Induced Injury Through Involvement of Glucocorticoids

et al. 2021

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Remote ischemic preconditioning (RIPC) is one of the most effective approaches to attenuate tissue injury caused by severe ischemia-reperfusion (I/R). Experimental studies have demonstrated that RIPC is capable of producing a protective effect not only on heart, but also on brain, lungs, kidneys, liver, intestine, and stomach. We previously demonstrated that glucocorticoids participate in protective effect of local gastric ischemic preconditioning against I/R-induced gastric injury. In the present study we investigated whether RIPC may protect the gastric mucosa against I/R-induced injury through involvement of glucocorticoids. Anesthetized fasted Sprague Dawley male rats were exposed to prolonged gastric I/R (30 min occlusion of celiac artery followed by 3 h of reperfusion) alone or with preliminary brief RIPC (10 min non-invasive occlusion of right hind limb blood flow followed by reperfusion for 30 min). First, we investigated the effect of RIPC on I/R-induced injury by itself. Then to study the role of glucocorticoids similar experiments were carried out: 1) in rats pretreated with the inhibitor of glucocorticoid synthesis, metyrapone (30 mg/kg, i.p), and in control animals; 2) in adrenalectomized rats without or with corticosterone replacement (4 mg/kg, s.c.) and in sham-operated animals; 3) in rats pretreated with glucocorticoid receptor antagonist RU-38486 (20 mg/kg, s.c.) and in control animals. I/R induced corticosterone rise and resulted in the gastric erosion formation. RIPC significantly reduced the erosion area in control animals. Metyrapone injected shortly before RIPC caused a decrease in plasma corticosterone levels and prevented the gastroprotective effect of RIPC and, moreover, further aggravated the deleterious effect of I/R. Adrenalectomy performed 1 week before experiment created long-lasting corticosterone deficiency and had no effect on the gastroprotective effect of RIPC. Nevertheless, corticosterone replacement which mimics the corticosterone rise, similar to RIPS, significantly reduced erosion areas of gastric mucosa in adrenalectomized rats supporting the role of glucocorticoids in gastroprotection. RU-38486, which occupied glucocorticoid receptors, similar to metyrapone prevented the gastroprotective effect of RIPC and, moreover, further aggravated the deleterious effect of I/R. The results of the present study demonstrate for the first time that RIPC may protect the gastric mucosa against I/R-induced injury through involvement of glucocorticoids.

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Section: Introductionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Non-Invasive Remote Ischemic Preconditioning May Protect the Gastric Mucosa Against Ischemia-Reperfusion-Induced Injury Through Involvement of Glucocorticoids

et al. 2021

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“…The gastroprotective effect of CRF was also prevented by the pretreatment of rats with RU-38486. The results obtained suggest that CRF-induced glucocorticoids contribute to gastroprotective action of CRF [ 69 ]. The findings further support the idea about gastroprotective role of stress-produced glucocorticoids.…”

Section: The Hpa Axis As a Hormonal Branch Of The Brain-gut Interactimentioning

confidence: 99%

The Realization of the Brain-Gut Interactions with Corticotropin-Releasing Factor and Glucocorticoids

Filaretova

Bagaeva²

2016

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BackgroundThe brain and the gut interact bi-directionally through the brain-gut axis. The interaction is mediated by the autonomic nervous system and the hypothalamic-pituitary-adrenocortical (HPA) system. The first brilliant demonstration of the brain-gut interactions was the cephalic phase of gastric and pancreatic secretion discovered by Ivan Pavlov, the first physiologist who was awarded the Nobel Prize for Physiology or Medicine in 1904. This review aims to identify the HPA system as a key hormonal branch of the brain-gut axis in stress.MethodsWe first outlined main components of the brain-gut axis and then focused on the HPA system as a key hormonal branch of the brain-gut axis in stress. We undertook a structured search of bibliographic databases for peer-reviewed research literature using a focused review question.ResultsSeventy-one articles were included in the review, the eleventh of them were articles of Filaretova L. and co-authors. We will discuss in our articles how an endocrinological approach to gastroenterological field can advance our understanding of the HPA axis role in regulation of gastric mucosal integrity and uncover new findings. According to these findings activation of the HPA system is gastroprotective component of the brain-gut axis in stress but not ulcerogenic one as it was generally accepted. Corticotropin-releasing factor (CRF) and glucocorticoids are important natural players provided gastroprotection. The results suggest that an initial action of endogenous glucocorticoids, including stress- and CRF-produced ones, as well as exogenous glucocorticoids, even used at pharmacological doses, is physiological gastroprotective. Prolongation of the hormonal action may lead to the transformation of gastroprotective hormonal effect to proulcerogenic one.ConclusionThe findings of this review demonstrate that corticotropin-releasing factor and glucocorticoids contribute to the realization of the brain-gut interactions and that activation of the HPA system is gastroprotective component of this interaction in stress.

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“…It is important to understand the mechanism by which stress‐induced gastric injury develops because it may be useful for the prevention and treatment of stress‐related organ injury. Several factors are known to play a role in the development of stress‐induced gastric injury, including reactive oxygen species, bioactive amines, and cytokines 1–3 . Although a variety of pro‐inflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, and IL‐18, are upregulated in the stomach after stress treatment, 4–6 the functional role of these cytokines in the development of stress‐induced gastric injury is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Role of nucleotide binding oligomerization domain‐like receptor protein 3 inflammasome in stress‐induced gastric injury

Higashimori

Watanabe

Nadatani

et al. 2020

J of Gastro and Hepatol

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Background and Aim The inflammasomes promote pro‐caspase‐1 cleavage, leading to processing of pro‐interleukin (IL)‐1β into its mature form. We investigated the role of the IL‐1β and nucleotide binding oligomerization domain‐like receptor protein 3 (NLRP3) inflammasome in gastric injury in mice receiving water‐immersion restraint stress (WIRS), focusing on the cyclooxygenase (COX)‐2/prostaglandin (PG) E2 axis. Methods To induce gastric injury, the mice were placed in a restraint cage and immersed in the water bath to the level of the xiphoid process. Protein levels of mature caspase‐1 and IL‐1β were assessed by western blotting. Results Water‐immersion restraint stress induced gastric injury with increase in IL‐1β expression by activation of NLRP3 inflammasome. Exogenous IL‐1β attenuated the injury, whereas anti‐IL‐1β neutralizing antibody and IL‐1β receptor antibody aggravated it. NLRP3−/− and caspase‐1−/− mice enhanced the injury with reducing of mature IL‐1β, and this aggravation was reduced by exogenous IL‐1β supplementation. Toll‐like receptor 4−/− mice were hyporesponsive to WIRS in terms of mature IL‐1β production. Rabeprazole attenuated the injury with preventing inflammasome activation. WIRS injured the stomach with promotion of COX‐2 mRNA and PGE2 production, and exogenous IL‐1β enhanced these molecules, while IL‐1β immunoneutralization exerted opposite effect. PGE2 supplementation abolished the hypersensitivity in NLRP3−/− and caspase‐1−/− mice through negative regulation of inflammatory cytokines. Conclusion These results suggest that NLRP3 inflammasome‐derived IL‐1β plays a protective role in stress‐induced gastric injury via activation of the COX‐2/PGE2 axis. Toll‐like receptor 4 signaling and gastric acid may be involved in NLRP3 inflammasome activation.

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Stress and the Stomach: Corticotropin-Releasing Factor May Protect the Gastric Mucosa in Stress Through Involvement of Glucocorticoids

Cited by 18 publications

References 28 publications

Non-Invasive Remote Ischemic Preconditioning May Protect the Gastric Mucosa Against Ischemia-Reperfusion-Induced Injury Through Involvement of Glucocorticoids

Non-Invasive Remote Ischemic Preconditioning May Protect the Gastric Mucosa Against Ischemia-Reperfusion-Induced Injury Through Involvement of Glucocorticoids

The Realization of the Brain-Gut Interactions with Corticotropin-Releasing Factor and Glucocorticoids

Role of nucleotide binding oligomerization domain‐like receptor protein 3 inflammasome in stress‐induced gastric injury

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