The effect of antioxidant supplementation on bacterial translocation after intestinal ischemia and reperfusion

Tassopoulos, Andreas; Chalkias, Athanasios; Papalois, Αpostolos; Iacovidou, Nicoletta; Xanthos, Theodoros

doi:10.1080/13510002.2016.1229893

Cited by 37 publications

(35 citation statements)

References 76 publications

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“…Transmigration is supported by weakened interactions between adjacent endothelial cells [65]. MPO is regarded as an important modulator of vasculature functioning, being associated with chronic vascular diseases such as atherosclerosis and chronic coronary disease [66]. After being released, MPO interaction with the vasculature is supported by electrostatic forces between positively charged MPO and negatively charged heparin-sulfate proteoglycans (HSPG) associated with the endothelium and negatively charged albumin [67,68] (Fig.…”

Section: Mpo and The Vasculaturementioning

confidence: 99%

Myeloperoxidase: A new player in autoimmunity

Strzępa

Pritchard

Dittel

2017

Cellular Immunology

182

103

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Myeloperoxidase (MPO) is the most toxic enzyme found in the azurophilic granules of neutrophils. MPO utilizes H2O2 to generate hypochlorous acid (HClO) and other reactive moieties, which kill pathogens during infections. In contrast, in the setting of sterile inflammation, MPO and MPO-derived oxidants are thought to be pathogenic, promoting inflammation and causing tissue damage. In contrast, evidence also exists that MPO can limit the extent of immune responses. Elevated MPO levels and activity are observed in a number of autoimmune diseases including in the central nervous system (CNS) of multiple sclerosis (MS) and the joints of rheumatoid arthritis (RA) patients. A pathogenic role for MPO in driving autoimmune inflammation was demonstrated using mouse models. Mechanisms whereby MPO is thought to contribute to disease pathogenesis include tuning of adaptive immune responses and/or the induction of vascular permeability.

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Section: Mpo and The Vasculaturementioning

confidence: 99%

Myeloperoxidase: A new player in autoimmunity

Strzępa

Pritchard

Dittel

2017

Cellular Immunology

182

103

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“…Human intestinal flora produces a considerable amount of endotoxins but the endothelial cell lining in intestines restrict the transfer of these endotoxins into circulation and prevent the systemic inflammation in normal conditions. In the course of major surgical procedures including cardiac surgery with cardiopulmonary bypass and aortic aneurysm repair, the disruption of endothelial cell barrier may permit the passage of endotoxins through the mucosal epithelium to the adjacent tissues or distal organs and provoke a systemic inflammatory response leading to increased postoperative complications [3][4][5][6] .…”

Section: ■ Introductionmentioning

confidence: 99%

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats

et al. 2020

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Design of the study, acquisition and analysis of data, final approval. ORIGINAL ARTICLE Experimental SurgeryActa Cir Bras. 2020;35(2):e202000202 AbstractPurpose: To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury.Methods: Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination.Results: Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05). Conclusions:Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.

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“…The reperfusion of a specific organ following blood flow obstruction or reduction may cause severe damage to this organ, and the small intestine is one of organs susceptible to I/R injury 2. The ischemia and/or inflammation may induce the excess production of reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

“…The ischemia and/or inflammation may induce the excess production of reactive oxygen species (ROS). Some ROS such as hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) are not only important signal molecules in cells, but also toxic to cells 2. Of these ROS, hydroxyl radical and peroxynitrite are the most toxic and mediate the oxidative damage to cells 34.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of hydrogen rich water on the intestinal ischemia/reperfusion injury due to intestinal intussusception in a rat model

Chen

Sang

et al. 2017

Med Gas Res

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This study aimed to investigate the protective effects of hydrogen rich water on the intestinal ischemia/reperfusion (I/R) injury in a rat intestinal intussusception (II) model. Ninety Sprague-Dawley rats were randomly assigned into three groups (n = 30 per group). In sham group, rats received laparotomy, and the intestine was exposed for 15 minutes without II. In I/R + saline group and I/R + hydrogen group, rats received II after laparotomy and then intestine was relocated 8 hours later, followed by immediately intraperitoneal injection of normal saline and hydrogen rich water (HRW) (5 mL/kg), respectively. One hour later, the intestine was collected for hematoxylin-eosin staining and immunohistochemistry for apoptotic cells and 8-oxo-deoxyguanosine, and blood was harvested for detection of tumor necrosis factor-α, malondialdehyde and superoxide dismutase. Hematoxylin-eosin staining showed the intestinal mucosa was significantly damaged in I/R + saline group, which was markedly attenuated after HRW treatment. The serum tumor necrosis factor-α content increased significantly in I/R + saline group, but HRW treatment reduced serum tumor necrosis factor-α content as compared to I/R + saline group (P < 0.05). Serum malondialdehyde content and 8-oxo-deoxyguanosine positive cells in the intestine increased dramatically after II, but HRW significantly reduced them in I/R+hydrogen group (P < 0.05). In addition, superoxide dismutase activity reduced markedly and apoptotic cells increased in I/R + saline group as compared to sham group, but they HRW increased superoxide dismutase activity and reduced apoptotic cells significantly in I/R + hydrogen group (P < 0.05). Our results indicate hydrogen rich water is able to attenuate II induced intestinal I/R injury via inhibiting intestinal inflammation, attenuating intestinal/serum oxidative stress and reducing apoptotic intestinal cells.

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The effect of antioxidant supplementation on bacterial translocation after intestinal ischemia and reperfusion

Cited by 37 publications

References 76 publications

Myeloperoxidase: A new player in autoimmunity

Myeloperoxidase: A new player in autoimmunity

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats

Protective effects of hydrogen rich water on the intestinal ischemia/reperfusion injury due to intestinal intussusception in a rat model

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