Oxidative gastric mucosal damage induced by ischemia/reperfusion and the mechanisms of its prevention by carbon monoxide-releasing tricarbonyldichlororuthenium (II) dimer

Magierowska, Katarzyna; Korbut, Edyta; Hubalewska-Mazgaj, Magdalena; Surmiak, Marcin; Chmura, Anna; Bakalarz, Dominik; Buszewicz, Grzegorz; Wójcik, Dagmara; Śliwowski, Zbigniew; Ginter, Grzegorz; Gromowski, Tomasz; Kwiecień, Sławomir; Brzozowski, Tomasz; Magierowski, Marcin

doi:10.1016/j.freeradbiomed.2019.09.032

Cited by 41 publications

(34 citation statements)

References 38 publications

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“…Digital documentation of histological slides was obtained using the abovementioned microscope equipped with automatic scanning table and ZEN Pro 2.3 software (Carl Zeiss, Oberkochen, Germany) to collect multiple photographs of each histological sample and to stitch them into one picture; to obtain better quality of each picture, the background was subtracted and unified as white [43]. Esophageal mucosal samples were collected for biochemical and molecular assessments on ice, snap-frozen in liquid nitrogen and stored at −80 • C until further analysis [43]. Blood samples were collected from the vena cava and serum was stored at −80 • C until further analysis [43].…”

Section: Animal Model Of Bementioning

confidence: 99%

“…Esophageal mucosal samples were collected for biochemical and molecular assessments on ice, snap-frozen in liquid nitrogen and stored at −80 • C until further analysis [43]. Blood samples were collected from the vena cava and serum was stored at −80 • C until further analysis [43].…”

Section: Animal Model Of Bementioning

confidence: 99%

“…Serum concentration of IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, TNF-α, IFN-γ, GM-CSF was assessed using the Luminex microbeads fluorescent assays (Bio-Rad, Hercules, CA, USA) and Luminex MAGPIX System (Luminex Corp., Austin, TX, USA). Results were calculated from the calibration curves and expressed in pg/mL, according to the manufacturer's protocol, as described previously [43].…”

Section: Determination Of Serum Content Of Pro-and Anti-inflammatory mentioning

confidence: 99%

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Molecular Profile of Barrett’s Esophagus and Gastroesophageal Reflux Disease in the Development of Translational Physiological and Pharmacological Studies

Korbut

Janmaat

Wierdak

et al. 2020

IJMS

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Barrett’s esophagus (BE) is a premalignant condition caused by gastroesophageal reflux disease (GERD), where physiological squamous epithelium is replaced by columnar epithelium. Several in vivo and in vitro BE models were developed with questionable translational relevance when implemented separately. Therefore, we aimed to screen Gene Expression Omnibus 2R (GEO2R) databases to establish whether clinical BE molecular profile was comparable with animal and optimized human esophageal squamous cell lines-based in vitro models. The GEO2R tool and selected databases were used to establish human BE molecular profile. BE-specific mRNAs in human esophageal cell lines (Het-1A and EPC2) were determined after one, three and/or six-day treatment with acidified medium (pH 5.0) and/or 50 and 100 µM bile mixture (BM). Wistar rats underwent microsurgical procedures to generate esophagogastroduodenal anastomosis (EGDA) leading to BE. BE-specific genes (keratin (KRT)1, KRT4, KRT5, KRT6A, KRT13, KRT14, KRT15, KRT16, KRT23, KRT24, KRT7, KRT8, KRT18, KRT20, trefoil factor (TFF)1, TFF2, TFF3, villin (VIL)1, mucin (MUC)2, MUC3A/B, MUC5B, MUC6 and MUC13) mRNA expression was assessed by real-time PCR. Pro/anti-inflammatory factors (interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, tumor necrosis factor α, interferon γ, granulocyte-macrophage colony-stimulating factor) serum concentration was assessed by a Luminex assay. Expression profile in vivo reflected about 45% of clinical BE with accompanied inflammatory response. Six-day treatment with 100 µM BM (pH 5.0) altered gene expression in vitro reflecting in 73% human BE profile and making this the most reliable in vitro tool taking into account two tested cell lines. Our optimized and established combined in vitro and in vivo BE models can improve further physiological and pharmacological studies testing pathomechanisms and novel therapeutic targets of this disorder.

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Section: Animal Model Of Bementioning

confidence: 99%

Section: Animal Model Of Bementioning

confidence: 99%

Section: Determination Of Serum Content Of Pro-and Anti-inflammatory mentioning

confidence: 99%

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Molecular Profile of Barrett’s Esophagus and Gastroesophageal Reflux Disease in the Development of Translational Physiological and Pharmacological Studies

Korbut

Janmaat

Wierdak

et al. 2020

IJMS

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“…Anti-inflammatory decreased serum level of TNF-α and IL-1β and expression of mRNA in gastric mucosa [5,15] inhibited production of TNF-α, IL-1β in LPS-stimulated macrophages in vivo and in vitro [44] reduced mRNA and protein expression of HIF-1α in gastric mucosa [5,15] increased IL-10 expression in macrophages via activation p38MAPK [87] supressed NF-κB pathway in gastric mucosa [21] decreased ERK1/2 kinase activity in T cells [88] induced activation of AnxA1 pathway [21] re reduced mRNA and protein expression of HIF-1α in gastric mucosa and supressed NF-κB pathway in gastric mucosa [15] involved in regulation of Th1, Th2, and Th17 lymphocyte differentiation, decrease of IL-17A content [50] Anti-oxidative caused Nrf-2 /HMOX-1pathway upregulation [11,18] inhibited the lipid peroxidation [2] decreased level of MDA and increased production of glutathione (GSH) [7,56] decreased level of MDA and modulated SOD activity [56,89] Vasodilatation increased gastric microcirculation via sGC on endogenous NO and CO biosynthesis-dependent manner [53,54,56] Increased gastric microcirculation via sGC with contribution of NO biosynthesis pathway and independently on endogenous H 2 S activity [40,42,43,54,56] dependent on activation of K ATP channels [90] dependent on activation of K ATP channels [91] HCO 3 secretion in duodenum increased [64] increased [62,64] Impact on gut microbiota caused the reconstitution of microbiota biofilm dysbiosis [69,72] found to be involved in CO/HMOX-1 pathway in cross-talk between the microbiota and the mucosal immune compartment [49]…”

Section: Beneficial Effects Of H 2 S and Comentioning

confidence: 99%

Synergisms, Discrepancies and Interactions between Hydrogen Sulfide and Carbon Monoxide in the Gastrointestinal and Digestive System Physiology, Pathophysiology and Pharmacology

2020

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Endogenous gas transmitters, hydrogen sulfide (H2S), carbon monoxide (CO) and nitric oxide (NO) are important signaling molecules known to exert multiple biological functions. In recent years, the role of H2S, CO and NO in regulation of cardiovascular, neuronal and digestive systems physiology and pathophysiology has been emphasized. Possible link between these gaseous mediators and multiple diseases as well as potential therapeutic applications has attracted great attention from biomedical scientists working in many fields of biomedicine. Thus, various pharmacological tools with ability to release CO or H2S were developed and implemented in experimental animal in vivo and in vitro models of many disorders and preliminary human studies. This review was designed to review signaling functions, similarities, dissimilarities and a possible cross-talk between H2S and CO produced endogenously or released from chemical donors, with special emphasis on gastrointestinal digestive system pathologies prevention and treatment.

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“…Nevertheless, CORM-2mediated gastroprotection and acceleration of ulcer healing was independent of H 2 S biosynthesis while NaHS was not effective when endogenous CO production was pharmacologically inhibited [34,35]. It is worth to mention that CO and H 2 S donors were reported to protect the GI tract against acute oxidative damage induced by ischemia/reperfusion (I/R) injury [36,37]. However, the NO/constitutive nitric oxide synthase (cNOS) pathway was shown to prevent I/Rinduced gastric lesions while the activation of the NO/inducible nitric oxide synthase (iNOS) molecular pathway activity exacerbated this damage [38].…”

Section: Co and Other Gaseous Mediators In Regulation Ofmentioning

confidence: 99%

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

Korbut

Brzozowski

Magierowski

2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress reflects an imbalance between oxidants and antioxidants in favor of the oxidants capable of evoking tissue damage. Like hydrogen sulfide (H2S) and nitric oxide (NO), carbon monoxide (CO) is an endogenous gaseous mediator recently implicated in the physiology of the gastrointestinal (GI) tract. CO is produced in mammalian tissues as a byproduct of heme degradation catalyzed by the heme oxygenase (HO) enzymes. Among the three enzymatic isoforms, heme oxygenase-1 (HO-1) is induced under conditions of oxidative stress or tissue injury and plays a beneficial role in the mechanism of protection against inflammation, ischemia/reperfusion (I/R), and many other injuries. According to recently published data, increased endogenous CO production by inducible HO-1, its delivery by novel pharmacological CO-releasing agents, or even the direct inhalation of CO has been considered a promising alternative in future experimental and clinical therapies against various GI disorders. However, the exact mechanisms underlying behind these CO-mediated beneficial actions are not fully explained and experimental as well as clinical studies on the mechanism of CO-induced protection are awaited. For instance, in a variety of experimental models related to gastric mucosal damage, HO-1/CO pathway and CO-releasing agents seem to prevent gastric damage mainly by reduction of lipid peroxidation and/or increased level of enzymatic antioxidants, such as superoxide dismutase (SOD) or glutathione peroxidase (GPx). Many studies have also revealed that HO-1/CO can serve as a potential defensive pathway against oxidative stress observed in the liver and pancreas. Moreover, increased CO levels after treatment with CO donors have been reported to protect the gut against formation of acute GI lesions mainly by the regulation of reactive oxygen species (ROS) production and the antioxidative activity. In this review, we focused on the role of H2S and NO molecular sibling, CO/HO pathway, and therapeutic potential of CO-releasing pharmacological tools in the regulation of oxidative stress-induced damage within the GI tract with a special emphasis on the esophagus, stomach, and intestines and also two solid and important metabolic abdominal organs, the liver and pancreas.

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Oxidative gastric mucosal damage induced by ischemia/reperfusion and the mechanisms of its prevention by carbon monoxide-releasing tricarbonyldichlororuthenium (II) dimer

Cited by 41 publications

References 38 publications

Molecular Profile of Barrett’s Esophagus and Gastroesophageal Reflux Disease in the Development of Translational Physiological and Pharmacological Studies

Molecular Profile of Barrett’s Esophagus and Gastroesophageal Reflux Disease in the Development of Translational Physiological and Pharmacological Studies

Synergisms, Discrepancies and Interactions between Hydrogen Sulfide and Carbon Monoxide in the Gastrointestinal and Digestive System Physiology, Pathophysiology and Pharmacology

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

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