Endogenous Hydrogen Sulfide Is an Anti-inflammatory Molecule in Dextran Sodium Sulfate-Induced Colitis in Mice

Hirata, Ikuhiro; Naito, Yuji; Takagi, Tomohisa; Mizushima, Katsura; Suzuki, Takahiro; Omatsu, Tatsushi; Handa, Osamu; Ichikawa, Hiroshi; Ueda, Hideo; Yoshikawa, Toshikazu

doi:10.1007/s10620-010-1461-5

Cited by 63 publications

(71 citation statements)

References 36 publications

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“…In dextran sulfate-induced ulcerative colitis in rats, administration of a sulfide binding compound, bismuth subsalicylate, reduced fecal sulfide release but did not protect against colitis, indicating that elevated sulfide does not play a role in the etiology of colitis, at least in this model [214]. On the other hand, other studies have reported a protective role for H 2 S in healing of gastric ulcers and colitis [215,216], gastric injury caused by anti-inflammatory nonsteroidal drugs [164] and resolution of colitis [168]. It is important to note that experimental models of ulcerative colitis might be substantially different from the naturally occurring disease and the effect of H 2 S could be dependent on both the experimental model as well as the stage of colitis.…”

Section: Cellular and Physiological Processes Regulated By H2smentioning

confidence: 95%

H2S and its role in redox signaling

Kabil

Motl

Banerjee

2014

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

194

148

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Hydrogen sulfide (H2S) has emerged as an important gaseous signaling molecule that is produced endogenously by enzymes in the sulfur metabolic network. H2S exerts its effects on multiple physiological processes important under both normal and pathological conditions. These functions include neuromodulation, regulation of blood pressure and cardiac function, inflammation, cellular energetics and apoptosis. Despite the recognition of its biological importance and its beneficial effects, the mechanism of H2S action and the regulation of its tissue levels remain unclear in part owing to its chemical and physical properties that render handling and analysis challenging. Furthermore, the multitude of potential H2S effects has made it difficult to dissect its signaling mechanism and to identify specific targets. In this review, we focus on H2S metabolism and provide an overview of the recent literature that sheds some light on its mechanism of action in cellular redox signaling in health and disease. This article is part of a Special Issue entitled: Thiol-Based Redox Processes.

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Section: Cellular and Physiological Processes Regulated By H2smentioning

confidence: 95%

H2S and its role in redox signaling

Kabil

Motl

Banerjee

2014

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

194

148

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“…Indeed, there remains conflicting evidence regarding the precise role of H 2 S in the gut[344,347]. On one hand, it appears that lower concentrations of endogenously derived H 2 S exert beneficial cytoprotective, antioxidant and anti-inflammatory actions[344,348–351], while on the other, increased H 2 S formation by SRB can promote oxidant formation, impair colonic epithelial H 2 S detoxification and induce cytotoxicity and disruption of intestinal barrier integrity, thereby driving local and systemic inflammation[344,347,352,353]. Certainly, further understanding of the roles that H 2 S concentration, substrate, and location play in inflammation and nitrate metabolism remain to be more fully elucidated.…”

Section: Dysbiosis Of the Microbiome In Pulmonary Hypertension And Vascmentioning

confidence: 99%

Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health

Koch

Gladwin

Freeman

et al. 2017

Free Radical Biology and Medicine

141

127

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Recent insights into the bioactivation and signaling actions of inorganic, dietary nitrate and nitrite now suggest a critical role for the microbiome in the development of cardiac and pulmonary vascular diseases. Once thought to be the inert, end-products of endothelial-derived nitric oxide (NO) heme-oxidation, nitrate and nitrite are now considered major sources of exogenous NO that exhibit enhanced vasoactive signaling activity under conditions of hypoxia and stress. The bioavailability of nitrate and nitrite depend on the enzymatic reduction of nitrate to nitrite by a unique set of bacterial nitrate reductase enzymes possessed by specific bacterial populations in the mammalian mouth and gut. The pathogenesis of pulmonary hypertension (PH), obesity, hypertension and CVD are linked to defects in NO signaling, suggesting a role for commensal oral bacteria to shape the development of PH through the formation of nitrite, NO and other bioactive nitrogen oxides. Oral supplementation with inorganic nitrate or nitrate-containing foods exert pleiotropic, beneficial vascular effects in the setting of inflammation, endothelial dysfunction, ischemia-reperfusion injury and in pre-clinical models of PH, while traditional high-nitrate dietary patterns are associated with beneficial outcomes in hypertension, obesity and CVD. These observations highlight the potential of the microbiome in the development of novel nitrate- and nitrite-based therapeutics for PH, CVD and their risk factors.

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“…2). The widely used CSE inhibitor, dl -proparylglycine, for example, can increase disease severity in animal models of colitis [96], myocardial ischemia–reperfusion-induced injury [97], and also has anti-hyperalgesic effects [98] and has reported inflammatory as well as anti-inflammatory effects in rodent models [21]. These studies indicate that the inhibition of H 2 S biosynthetic enzymes, and therefore, the production of H 2 S within tissues and cells typically leads to increased disease severity which effects are reversed by the use of H 2 S donor molecules.…”

Section: Pharmacological Approaches To Manipulate H2s Levels Within Bmentioning

confidence: 99%

H2S biosynthesis and catabolism: new insights from molecular studies

Rose

Moore

Zhu

2016

Cell. Mol. Life Sci.

139

100

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Hydrogen sulfide (H2S) has profound biological effects within living organisms and is now increasingly being considered alongside other gaseous signalling molecules, such as nitric oxide (NO) and carbon monoxide (CO). Conventional use of pharmacological and molecular approaches has spawned a rapidly growing research field that has identified H2S as playing a functional role in cell-signalling and post-translational modifications. Recently, a number of laboratories have reported the use of siRNA methodologies and genetic mouse models to mimic the loss of function of genes involved in the biosynthesis and degradation of H2S within tissues. Studies utilising these systems are revealing new insights into the biology of H2S within the cardiovascular system, inflammatory disease, and in cell signalling. In light of this work, the current review will describe recent advances in H2S research made possible by the use of molecular approaches and genetic mouse models with perturbed capacities to generate or detoxify physiological levels of H2S gas within tissues.

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Endogenous Hydrogen Sulfide Is an Anti-inflammatory Molecule in Dextran Sodium Sulfate-Induced Colitis in Mice

Abstract: Taken together, the results indicated that the inhibition of endogenous H(2)S generation caused the deterioration of DSS-induced colitis. We conclude that physiological H(2)S might act as an anti-inflammatory molecule in colitis.

Cited by 63 publications

References 36 publications

H2S and its role in redox signaling

H2S and its role in redox signaling

Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health

H2S biosynthesis and catabolism: new insights from molecular studies

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