Marcin Magierowski

Jagiellonian University

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Tomasz Brzozowski

Jagiellonian University

Sławomir Kwiecień

Jagiellonian University

Katarzyna Magierowska

Jagiellonian University

Dagmara Wójcik

Jagiellonian University

ZŚ

Zbigniew Śliwowski

Jagiellonian University

Marcin Surmiak

Jagiellonian University

Agata Ptak‐Belowska

Jagiellonian University

Edyta Korbut

Jagiellonian University

Anna Chmura

Jagiellonian University

Katarzyna Jasnos

Population Health Research Institute

Cooperative Institutions

Jagiellonian University

Erasmus MC

Friedrich-Alexander-Universität Erlangen-Nürnberg

Cracow University of Technology

Maj Institute of Pharmacology

University School of Physical Education in Kraków

Universidade Federal do Piauí

Universidade Federal do Delta do Parnaíba

University of California, Irvine

Georgia State University

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834 EFFECT OF MATERNAL OBESITY INDUCED BY DIFFERENT DIET PROGRAM ON THE PLASMA LEVELS OF APPETITE HORMONES AND INTESTINAL EXPRESSION OF ADIPOKINES AND ADIPO RECEPTORS 1 AND 2 IN MALE AND FEMALE RAT OFFSPRING

Gastroenterology (2020)

Urszula Głowacka Kinga Gawlińska Dawid Gawliński Marcin Magierowski Zbigniew Śliwowski

Plasma levels

10.1016/s0016-5085(20)31104-5

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Cross-talk between hydrogen sulfide and carbon monoxide in the mechanism of experimental gastric ulcers healing, regulation of gastric blood flow and accompanying inflammation

Biochemical Pharmacology (2017)

Marcin Magierowski Katarzyna Magierowska Magdalena Hubalewska‐Mazgaj Marcin Surmiak Zbigniew Śliwowski

Zinc protoporphyrin

Hemin

10.1016/j.bcp.2017.11.020

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Citations (52)

The effect of hydrogen sulfide-releasing naproxen (ATB-346) versus naproxen on formation of stress-induced gastric lesions, the regulation of systemic inflammation, hypoxia and alterations in gastric microcirculation.

PubMed (2017)

Marcin Magierowski Katarzyna Magierowska Marcin Surmiak Magdalena Hubalewska‐Mazgaj Sławomir Kwiecień

Clinical use of non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin or naproxen is limited due to the gastrotoxicity evoked by these compounds. Endogenous hydrogen sulfide (H2s) and delivered via an H2s donor have been shown to play important role in the maintenance of gastric mucosal integrity. This study aimed to compare the effects of naproxen and an H2s-releasing naproxen derivative (ATB-346) on gastric lesion induction by water immersion and restraint stress (WRS), the alterations in gastric blood flow (GBF) and the influence of these drugs on systemic inflammation. Wistar rats were pretreated i.g. with vehicle, naproxen (20 mg/kg) or ATB-346 (equimolar dose) or NaHS (5 mg/kg), the H2s donor, combined with naproxen and exposed to 3.5 hours of WRS. The gastric lesion number and GBF were assessed by planimetry and laser Doppler flowmetry, respectively. Plasma concentrations of interleukins: IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and GM-CSF were determined by Luminex system and gastric mucosal protein expression of cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), hypoxia inducible factor-1α (HIF-1α), heme oxygenase-1 (HO-1) and cyclooxygenase (COX-2) were analyzed by Western blot. Pretreatment with naproxen increased the number of WRS stress-induced gastric lesions and significantly decreased GBF as compared with vehicle (p < 0.05). In contrast, pretreatment with ATB-346 or naproxen combined with NaHS significantly reduced WRS-lesions number and elevated GBF as compared with naproxen (p < 0.05). Naproxen significantly increased gastric mucosal protein expression of CSE, Nrf-2 and HIF-1α as compared with vehicle (p < 0.05), but failed to affect CBS, 3-MST and HO-1. ATB-346 significantly increased Nrf-2 and HO-1 protein expression as compared with vehicle (P < 0.05) but did not affect the protein expression of CSE, CBS, 3-MST or HIF-1α. ATB-346 but not naproxen decreased COX-2 protein expression in gastric mucosa compromised by WRS (p < 0.05). Exposure to WRS increased plasma concentration of all investigated cytokines (p < 0.05). ATB-346 but not naproxen decreased plasma content of IL-1α, IL-4, IL-5, IL-6, IL-10, IL-12, TNF-α and IFN-γ in rats exposed to WRS (p < 0.05). We conclude that H2s through its vasoactive properties attenuates the gastrotoxic effects of naproxen, which increased stress-induced hypoxia in gastric mucosa. In contrast to naproxen, ATB-346 decreased stress-induced systemic inflammation and pro-inflammatory COX-2 expression in the gastric mucosa. The decreased gastrotoxicity of ATB-346 could be due to upregulation of Nrf-2/HO-1 pathway mediated by the release of H2s.

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Sa1099 - Hydrogen Sulfide (H 2 S) Prevents Development of Barrett's Esophagus Metaplasia

Gastroenterology (2018)

Marcin Magierowski Mateusz Wierdak Katarzyna Magierowska Vincent T. Janmaat Magdalena Hubalewska‐Mazgaj

Barrett's esophagus

Metaplasia

10.1016/s0016-5085(18)31180-6

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Exploiting Significance of Physical Exercise in Prevention of Gastrointestinal Disorders

Current Pharmaceutical Design (2018)

Jan Bilski Agnieszka Mazur-Biały Marcin Magierowski Sławomir Kwiecień Dagmara Wójcik

Background: Physical activity can be involved in the prevention of gastrointestinal (GI)-tract diseases, however, the results regarding the volume and the intensity of exercise considered as beneficial for protection of gastrointestinal organs are conflicting. Aims and Methods: The main objective of this review is to provide a comprehensive and updated overview on the beneficial and harmful effects of physical activity on the gastrointestinal tract. We attempted to discuss recent evidence regarding the association between different modes and intensity levels of exercise and physiological functions of the gut and gut pathology. Results: The regular, moderate exercise can exert a beneficial effect on GI-tract disorders such as reflux esophagitis, peptic ulcers, cholelithiasis, constipation and Inflammatory Bowel Disease (IBD) leading to the attenuation of the symptoms. This voluntary exercise has been shown to reduce the risk of colorectal cancer. On the other hand, there is considerable evidence that the high-intensity training or prolonged endurance training can exert a negative influence on GI-tract resulting in the exacerbation of symptoms. Conclusion: Physical activity can exhibit a beneficial effect on a variety of gastrointestinal diseases, however, this effect depends upon the exercise mode, duration and intensity. The accumulated evidence indicate that management of gastrointestinal problems and their relief by the exercise seems to be complicated and require adjustments of physical activity training, dietary measures and medical monitoring of symptoms. More experimental and clinical studies on the effects of physical activity on GI-tract disorders are warranted. Especially, the association between the exercise intensity and data addressing the underlying mechanism(s) of the exercise as the complementary therapy in the treatment of gastrointestinal disorders, require further determination in animal models and humans.

Physical exercise

10.2174/1381612824666180522103759

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Citations (19)

Role of Gut-Adipose-muscle Axis in Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a Diet-Induced Obesity. Involvement of Protective Irisin and Proinflammatory Biomarkers Released from Mesenteric Fat and Colonic Mucosa

Gastroenterology (2017)

Jan Bilski Agnieszka Mazur-Biały Magdalena Hubalewska‐Mazgaj Bartosz Brzozowski Marcin Surmiak

Proinflammatory cytokine

Myokine

Turnover

10.1016/s0016-5085(17)32861-5

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Citations (2)

Mo1866 THERAPEUTIC ADMINISTRATION OF INTESTINAL ALKALINE PHOSPHATASE ALLEVIATES INFLAMMATION AND SHAPES THE COMPOSITION OF THE INTESTINAL MICROBIOTA IN MICE WITH ABDOMINAL ADIPOSITY AND EXPERIMENTAL COLITIS SUBJECTED TO FORCED TREADMILL EXERCISE

Gastroenterology (2023)

Dagmara Wójcik Zbigniew Śliwowski Sławomir Kwiecień Aneta Targosz Malgorzata Strzałka

Treadmill

10.1016/s0016-5085(23)03128-1

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Organic carbon monoxide prodrug, BW-CO-111, in protection against chemically-induced gastric mucosal damage

Acta Pharmaceutica Sinica B (2020)

Dominik Bakalarz Marcin Surmiak Xiaoxiao Yang Dagmara Wójcik Edyta Korbut

Metal-based carbon monoxide (CO)-releasing molecules have been shown to exert anti-inflammatory and anti-oxidative properties maintaining gastric mucosal integrity. We are interested in further development of metal-free CO-based therapeutics for oral administration. Thus, we examine the protective effect of representative CO prodrug, BW-CO-111, in rat models of gastric damage induced by necrotic ethanol or aspirin, a representative non-steroidal anti-inflammatory drug. Treatment effectiveness was assessed by measuring the microscopic/macroscopic gastric damage area and gastric blood flow by laser flowmetry. Gastric mucosal mRNA and/or protein expressions of HMOX1, HMOX2, nuclear factor erythroid 2-related factor 2, COX1, COX2, iNos, Anxa1 and serum contents of TGFB1, TGFB2, IL1B, IL2, IL4, IL5, IL6, IL10, IL12, tumor necrosis factor α, interferon γ, and GM-CSF were determined. CO content in gastric mucosa was assessed by gas chromatography. Pretreatment with BW-CO-111 (0.1 mg/kg, i.g.) increased gastric mucosal content of CO and reduced gastric lesions area in both models followed by increased GBF. These protective effects of the CO prodrug were supported by changes in expressions of molecular biomarkers. However, because the pathomechanisms of gastric damage differ between topical administration of ethanol and aspirin, the possible protective and anti-inflammatory mechanisms of BW-CO-111 may be somewhat different in these models.

10.1016/j.apsb.2020.08.005

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Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers

Nutrients (2017)

Agnieszka Mazur-Biały Jan Bilski Dagmara Wójcik Bartosz Brzozowski Marcin Surmiak

Inflammatory bowel diseases (IBDs) are a heterogeneous group of disorders exhibited by two major phenotypic forms: Crohn's disease and ulcerative colitis. Although the aetiology of IBD is unknown, several factors coming from the adipose tissue and skeletal muscles, such as cytokines, adipokines and myokines, were suggested in the pathogenesis of ulcerative colitis; however, it has not been extensively studied whether voluntary exercise can ameliorate that disorder. We explored the effect of moderate exercise (i.e., voluntary wheel running) on the disease activity index (DAI), colonic blood flow (CBF), plasma irisin and adiponectin levels and real-time PCR expression of proinflammatory markers in mesenteric fat in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS) colitis fed a high-fat diet (HFD) compared to those on a standard chow diet (SD). Macroscopic and microscopic colitis in sedentary SD mice was accompanied by a significant fall in CBF, some increase in colonic tissue weight and a significant increase in the plasma levels of tumour necrosis factor-alpha (TNF-α), IL-6, monocyte chemotactic protein 1 (MCP-1) and IL-13 (p < 0.05). In sedentary HFD mice, colonic lesions were aggravated, colonic tissue weight increased and the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels significantly increased. Simultaneously, a significant decrease in the plasma irisin and adiponectin levels was observed in comparison with SD mice (p < 0.05). Exercise significantly decreased macroscopic and microscopic colitis, substantially increased CBF and attenuated the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels while raising the plasma irisin and the plasma and WAT concentrations of adiponectin in HFD mice (p < 0.05). We conclude that: (1) experimental colitis is exacerbated in HFD mice, possibly due to a fall in colonic microcirculation and an increase in the plasma and mesenteric fat content of proinflammatory biomarkers; and (2) voluntary physical activity can attenuate the severity of colonic damage in mice fed a HFD through the release of protective irisin and restoration of plasma adiponectin.

Proinflammatory cytokine

10.3390/nu9040410

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Citations (49)

Su1122 DEVELOPMENT OF BARRETT'S ESOPHAGUS (BE) AND GASTROESOPHAGEAL REFLUX DISEASE (GERD) EXPERIMENTAL MODELS FOR TRANSLATIONAL PHARMACOLOGICAL STUDIES RELATED TO THE POSSIBLE NOVEL TREATMENT METHODS OF THESE PATHOLOGIES

Gastroenterology (2020)

Edyta Korbut Mateusz Wierdak Jerzy Hankus Vincent T. Janmaat Dagmara Wójcik

Barrett's esophagus

10.1016/s0016-5085(20)31973-9

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Citations (0)