S-Nitrosothiols, Nitric Oxide and Proinflammatory Cytokines in Children with Inflammatory Bowel Disease

Коркоташвили, Л В; Yazykova, A B; Федулова, Э. Н.; Тутина, О. А.; Толкачева, Н. И.

doi:10.7754/clin.lab.2012.120632

Cited by 9 publications

(5 citation statements)

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“…115 Nitrosothiols are significantly increased in UC and CD in children. 119 Decreased endogenous antioxidants are evident in IBD patients, especially in periods of remission, 120 which suggests that increased O&NS and decreased antioxidants contribute to recurrent disease activity. For example, Alzoghaibi 121 reported lower blood levels of vitamins C and E and lowered intestinal mucosa concentrations of glutathione, β-carotene, and vitamin A, C, and E in CD patients.…”

Section: Inflammation and Cell-mediated Immune Activation In Ibdmentioning

confidence: 99%

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Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways

Anderson²,

et al. 2015

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The nature of depression has recently been reconceptualized, being conceived as the clinical expression of activated immune-inflammatory, oxidative, and nitrosative stress (IO&NS) pathways, including tryptophan catabolite (TRYCAT), autoimmune, and gut-brain pathways. IO&NS pathways are similarly integral to the pathogenesis of inflammatory bowel disease (IBD). The increased depression prevalence in IBD associates with a lower quality of life and increased morbidity in IBD, highlighting the role of depression in modulating the pathophysiology of IBD.This review covers data within such a wider conceptualization that better explains the heightened co-occurrence of IBD and depression. Common IO&NS underpinning between both disorders is evidenced by increased pro-inflammatory cytokine levels, eg, interleukin-1 (IL-1) and tumor necrosis factor-α, IL-6 trans-signalling; Th-1-and Th-17-like responses; neopterin and soluble IL-2 receptor levels; positive acute phase reactants (haptoglobin and C-reactive protein); lowered levels of negative acute phase reactants (albumin, transferrin, zinc) and anti-inflammatory cytokines (IL-10 and transforming growth factor-β); increased O&NS with damage to lipids, proteinsm and DNA; increased production of nitric oxide (NO) and inducible NO synthase; lowered plasma tryptophan but increased TRYCAT levels; autoimmune responses; and increased bacterial translocation. As such, heightened IO&NS processes in depression overlap with the biological underpinnings of IBD, potentially explaining their increased co-occurrence. This supports the perspective that there is a spectrum of IO&NS disorders that includes depression, both as an emergent comorbidity and as a contributor to IO&NS processes. Such a frame of reference has treatment implications for IBD when "comorbid" with depression.

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Section: Inflammation and Cell-mediated Immune Activation In Ibdmentioning

confidence: 99%

“…Other ROS pathways are also involved in the pathology of IBD, including xanthine oxidase, 5-lypoxigenase, and cytochrome P450 enzymes 115 . Nitrosothiols are significantly increased in UC and CD in children 119 …”

Section: Inflammation and Oxidative And Nitrosative Stress (Ioandns) Pamentioning

confidence: 99%

Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways

Anderson²,

et al. 2015

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“…Excess nitric oxide (NO) generation is a sign of the inflammatory response 40 . Pro-inflammatory cytokines, such as IL-6 and TNF-α, have been recognized as critical regulators in inflammatory diseases 41 such as rheumatoid arthritis 42 , inflammatory bowel disease 43 , asthma 44 , and diabetic complications 45 . Inhibiting the release of pro-inflammatory cytokines is an important mode of action for anti-inflammatory drugs 46 .…”

Section: Resultsmentioning

confidence: 99%

Discovery, total syntheses and potent anti-inflammatory activity of pyrrolinone-fused benzoazepine alkaloids Asperazepanones A and B from Aspergillus candidus

Guo

Zhang

et al. 2022

Commun Chem

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Natural products are well established as an important resource and play an important role in drug discovery. Here, two pyrrolinone-fused benzoazepine alkaloids, (+)-asperazepanones A (1) and B (2) with a 6/7/5 ring system, together with the artifact (−)-asperazepanone A (1), were isolated from the coral-derived Aspergillus candidus fungus. Their structures including absolute configurations were elucidated by extensive spectroscopic methods, single crystal X-ray diffraction, and ECD calculations. Furthermore, total syntheses of (±)-1 and (±)-2 have been achieved starting from the commercially L-aspartic acid diethyl ester hydrochloride and monoethyl malonate in 7 and 8 steps, respectively. The key step in the syntheses was an intramolecular Friedel-Crafts reaction to build the unique tricyclic skeleton. Interestingly, (+)-2 not only showed obviously inhibitory activity against NO production, but also inhibited potent LPS-induced expression of TNF-α and IL-6 at the concentration of 0.1 μM. It thus represents a potentially promising lead for anti-inflammatory drug discovery.

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“…This study aimed to detail the mechanisms of the OP-D-induced treatment effects on colitis. Studies have shown that the NF-κB pathway is related to all factors, including in ammation, the oxidative stress, apoptosis, and the recovery of the barrier function of intestines [33]. NF-κB activation is required for apoptosis in brocystin/polyductin-depleted kidney epithelial cells, and CFTR ameliorates high glucose-induced oxidative stress and in ammation by mediating the NF-κB and MAPK signaling pathways in endothelial cells as well as arsenic downregulates tight junction claudin proteins through p38 and NF-κB in the intestinal epithelial cell line, HT-29 [34,10,35].…”

Section: Discussionmentioning

confidence: 99%

Ophiopogonin D Inhibiting Epithelial NF-κB Signaling Pathway Protects Against Experimental Colitis in Mice

et al. 2022

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The sustained activation of the nuclear factor κB (NF-κB) signaling pathway has been observed in human in ammatory bowel disease (IBD). Ophiopogonin D (OP-D) is a small molecular compound isolated from Ophiopogon japonicus, a widely used herbal remedy. In this study, dextran sodium sulfate was used to make a mouse model of experimental colitis and verify the effect of OP-D on the mouse model of experimental colitis. Small molecule-protein molecular docking approaches were also used to discover the mechanisms underlying the OP-D-induced regulation of colitis.In colitis, the OP-D can inhibit the apoptosis of intestinal mucosa cells, restore the intestinal barrier, and alleviate in ammation. The molecular docking simulations showed that OP-D had a high a nity with the REL-homology domain of NF-κB-p65 that affected its translocation to the nucleus. In a cell study, the effects of OP-D on in ammation and barrier dysfunction were signi cantly decreased by a small interfering RNA targeting NF-κB-p65. Further, the LPS-induced increase in NF-κB-p65 in the nucleus was also signi cantly inhibited by OP-D. OP-D alleviated experimental colitis by inhibiting NF-κB. New insights into the pathogenesis and treatment options of colitis are provided though this study.

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S-Nitrosothiols, Nitric Oxide and Proinflammatory Cytokines in Children with Inflammatory Bowel Disease

Cited by 9 publications

References 0 publications

Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways

Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways

Discovery, total syntheses and potent anti-inflammatory activity of pyrrolinone-fused benzoazepine alkaloids Asperazepanones A and B from Aspergillus candidus

Ophiopogonin D Inhibiting Epithelial NF-κB Signaling Pathway Protects Against Experimental Colitis in Mice

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