Endogenous hydrogen sulfide reduces airway inflammation and remodeling in a rat model of asthma

Chen, Yahong; Wu, Rui; Geng, Bin; Qi, Yongcheng; Wang, Peipei; Yao, Wan-zhen; Tang, Chaoshu

doi:10.1016/j.cyto.2008.11.009

Cited by 146 publications

(121 citation statements)

References 28 publications

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“…NaSH (14 µmol/kg, intraperitoneal) significantly improved lung function (peak expiratory flow, peak inspiratory flow, intrapressure and maximum rising slope of intrapressure) and inhibited iNOS activation in the lung [64] Male C57B1/6 mice and male Wistar rats: Acute inflammation of the knee induced by kaolin-carrageenan S decreased synovial blood flow but had no effect on joint pain [69] Female C57BL/6 mice: Acute lung injury; B + S injury GYY4137 also decreased LPS-induced hypotension [32] In vitro cellular study using murine RAW264.7 macrophages significantly decreased reduced lung inflammation to a significantly greater extent than diclofenac alone; however, ACS15 was ineffective against pancreatic injury (i.e., acinar cell death, pancreatic neutrophil accumulation or plasma amylase) [129] Rats: OA-induced acute -independent oxidative burst [132] In vitro cellular study formyl-methionyl-leucylphenylalanine-and zymosan-activated serum stimulated polymorphonuclear cells …”

Section: S-mediated Inhibition Of Inosmentioning

confidence: 97%

“…A role for H 2 S in asthma has also been investigated [64]. In normal rat lung tissue, CSE expression is located primarily in airway and vascular smooth muscle cells [64]. In the ovalbumin (OVA) challenge model of asthma in mice, OVA treatment reduced CSE expression and decreased pulmonary tissue H 2 S synthesis.…”

Section: H 2 S and Inflammatory Lung Diseasementioning

confidence: 99%

“…A role for H 2 S in asthma has also been investigated [64]. In normal rat lung tissue, CSE expression is located primarily in airway and vascular smooth muscle cells [64].…”

Section: H 2 S and Inflammatory Lung Diseasementioning

confidence: 99%

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Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Whiteman

Winyard

2011

Expert Review of Clinical Pharmacology

279

232

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Section: S-mediated Inhibition Of Inosmentioning

confidence: 97%

Section: H 2 S and Inflammatory Lung Diseasementioning

confidence: 99%

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Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Whiteman

Winyard

2011

Expert Review of Clinical Pharmacology

279

232

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“…So we tested the protein and mRNA expression of SUR2B and Kir6.1 in aortic and pulmonary arteries to investigate the possible mechanisms responsible for the regulation of vasorelaxation by H 2 S. H 2 S deficiency has been observed in animal models of systemic and pulmonary hypertension [16][17][18] . It also plays important roles in the pathogenesis of cardiovascular diseases [16][17][18][19][20][21][22][23][24] . The main mechanism for the cardiovascular actions of H 2 S was considered to be the activation of K ATP channels, because H 2 S increased whole-cell K ATP channel currents in rat aortic vascular smooth muscle cells [15] .…”

Section: Wwwchinapharcom Sun Y Et Almentioning

confidence: 99%

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

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Aim:To compare the vasorelaxing effects of hydrogen sulfide (H 2 S) on isolated aortic and pulmonary artery rings and to determine their action mechanisms. Methods: H 2 S-induced vasorelaxation of isolated rat aortic versus pulmonary artery rings under 95% O 2 and 5% CO 2 was analyzed. The expression of cystathinonine gamma-lyase (CSE), cystathionine beta synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST), SUR2B and Kir6.1 was examined. Results: NaHS caused vasorelaxation of rat aortic and pulmonary artery rings in a dose-dependent manner. NaHS dilated aortic rings to a greater extent (16.4%, 38.4%, 64.1%, 84.3%, and 95.9% at concentrations of 50, 100, 200, 500, and 1000 μmol/L, respectively) than pulmonary artery rings (10.1%, 22.2%, 50.6%, 73.6%, and 84.6% at concentrations of 50, 100, 200, 500 and 1000 μmol/L, respec tively). The EC 50 of the vasorelaxant effect for aortic rings was 152.17 μmol/L, whereas the EC 50 for pulmonary artery rings was 233.65 μmol/L. The vasorelaxing effect of H 2 S was markedly blocked b y cellular and mitochondrial membrane K ATP channel blockers in aortic rings (P<0.01). In contrast, only the cellular membrane K ATP channel blocker inhibited H 2 S-induced vasorelaxation in pulmonary artery rings. SUR2B mRNA and protein expression was higher in aortic rings than in pulmonary artery rings. Cystathinonine gamma-lyase (CSE) but not cystathionine beta synthase (CBS) expression in aortic rings was higher than in pulmonary artery rings. 3-Mercapto pyruvate sulfurtransferase (3MST) mRNA was lower in aortic rings than in pulmonary artery rings. Conclusion: The vasorelaxing effect of H 2 S on isolated aortic rings was more pronounced than the effect on pulmonary artery rings at specific concentrations, which might be associated with increased expression of the K ATP channel subunit SUR2B.

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“…Promotes SOD and catalase activities and reduces the production of malondialdehyde in oxidative lung injury [114]. Reduces lung inflammation and remodeling in asthmatic animals [115] and in pulmonary hypertension [116].…”

Section: Other Organ Effectsmentioning

confidence: 99%

The Oxidative Stress of Hyperhomocysteinemia Results from Reduced Bioavailability of Sulfur-Containing Reductants

Ingenbleek¹

2011

TOCCHEMJ

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Vegetarian subjects consuming subnormal amounts of methionine (Met) are characterized by subclinical protein malnutrition causing reduction in size of their lean body mass (LBM) best identified by the serial measurement of plasma transthyretin (TTR). As a result, the transsulfuration pathway is depressed at cystathionine--synthase (C S) level triggering the upstream sequestration of homocysteine (Hcy) in biological fluids and promoting its conversion to Met. Maintenance of beneficial Met homeostasis is counterpoised by the drop of cysteine (Cys) and glutathione (GSH) values downstream to C S causing in turn declining generation of hydrogen sulfide (H 2 S) from enzymatic sources. The biogenesis of H 2 S via non-enzymatic reduction is further inhibited in areas where earth's crust is depleted in elemental sulfur (S 8 ) and sulfate oxyanions. Combination of subclinical malnutrition and S 8 -deficiency thus maximizes the defective production of Cys, GSH and H 2 S reductants, explaining persistence of unabated oxidative burden. The clinical entity increases the risk of developing cardiovascular diseases (CVD) and stroke in underprivileged plant-eating populations regardless of Framingham criteria and vitamin-B status. Although unrecognized up to now, the nutritional disorder is one of the commonest worldwide, reaching top prevalence in populated regions of Southeastern Asia. Increased risk of hyperhomocysteinemia and oxidative stress may also affect individuals suffering from intestinal malabsorption or westernized communities having adopted vegan dietary lifestyles.

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Endogenous hydrogen sulfide reduces airway inflammation and remodeling in a rat model of asthma

Cited by 146 publications

References 28 publications

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The Oxidative Stress of Hyperhomocysteinemia Results from Reduced Bioavailability of Sulfur-Containing Reductants

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