Hydrogen sulfide protects rat lung from ischemia–reperfusion injury

Fu, Zhanli; Liu, Xinmin; Geng, Bin; Fang, Liping; Tang, Chaoshu

doi:10.1016/j.lfs.2008.04.005

Cited by 126 publications

(84 citation statements)

References 26 publications

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“…17 Other studies have shown the effects of inhibitors of CSE and CBS in ischemic models, but the specificity of these inhibitors is subject to discussion. 35 Most studies using these inhibitors imply protective effects afforded by endogenous H 2 S. 25,[36][37][38] Interestingly, recent data suggest that under stress, CSE can translocate to mitochondria, and H 2 S produced by mitochondrially located CSE can be used as a substrate for the production of ATP. 39 This might be an additional protective mechanism in the setting of ischemia/hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Cystathionine γ-Lyase Protects against Renal Ischemia/Reperfusion by Modulating Oxidative Stress

Bos

Wang

Snijder³

et al. 2013

Journal of the American Society of Nephrology

172

147

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Hydrogen sulfide (H 2 S) is an endogenous gasotransmitter with physiologic functions similar to nitric oxide and carbon monoxide. Exogenous treatment with H 2 S can induce a reversible hypometabolic state, which can protect organs from ischemia/reperfusion injury, but whether cystathionine g-lyase (CSE), which produces endogenous H 2 S, has similar protective effects is unknown. Here, human renal tissue revealed abundant expression of CSE, localized to glomeruli and the tubulointerstitium. Compared with wild-type mice, CSE knockout mice had markedly reduced renal production of H 2 S, and CSE deficiency associated with increased damage and mortality after renal ischemia/reperfusion injury. Treatment with exogenous H 2 S rescued CSE knockout mice from the injury and mortality associated with renal ischemia. In addition, overexpression of CSE in vitro reduced the amount of reactive oxygen species produced during stress. Last, the level of renal CSE mRNA at the time of organ procurement positively associated with GFR 14 days after transplantation. In summary, these results suggest that CSE protects against renal ischemia/reperfusion injury, likely by modulating oxidative stress through the production of H 2 S.

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Section: Discussionmentioning

confidence: 99%

Cystathionine γ-Lyase Protects against Renal Ischemia/Reperfusion by Modulating Oxidative Stress

Bos

Wang

Snijder³

et al. 2013

Journal of the American Society of Nephrology

172

147

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show abstract

“…[15][16][17][18] More recently, H 2 S has been shown to be protective in many models of tissue IRI, including brain, intestine, lung, liver and myocardium via a variety of antioxidant, anti-apoptotic and anti-inflammatory effects. [19][20][21][22][23] Using a rodent model of warm renal IRI involving uninephric renal clamping with clinically relevant, prolonged warm ischemic times, we have found that exogenous H 2 S treatment during warm renal IRI improves renal function and reduces IRIinduced inflammation in the acute recovery period. 24 To improve clinical outcomes following PN, H 2 S treatment must be shown to provide long-term improvement of renal function and resolution of inflammation.…”

Section: Introductionmentioning

confidence: 98%

Hydrogen sulfide treatment improves long-term renal dysfunction resulting from prolonged warm renal ischemia-reperfusion injury

Lobb

Zhu

Liu

et al. 2014

CUAJ

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“…4,[9][10][11][12] Studies have shown that H 2 S can ameliorate IRI in the heart, lung, liver, kidney and small intestine, and thus plays a general protective role against IR in different organs. [13][14][15][16][17] In a rat renal IRI model, H 2 S level was significantly decreased; however, administration of the exogenous H 2 S donor, NaHS, ameliorated IRI and improved renal function. 18 Similar observation has been obtained in living mice.…”

Section: Introductionmentioning

confidence: 99%

Impact of endogenous hydrogen sulfide on toll-like receptor pathway in renal ischemia/reperfusion injury in rats

et al. 2015

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In this study, we investigated the impact of endogenous hydrogen sulfide (H 2 S) on toll-like receptors (TLRs)-mediated inflammatory response and apoptosis in renal ischemia-reperfusion injury (IRI). Twenty-four male Wistar rats were randomly divided into four groups: sham, IR, IR + propargylglycine (PAG) and IR + hydroxylamine (HA). After right nephrectomy, rats were given saline for the sham and IR group, PAG for the IR + PAG group and HA for the IR + HA group, through the left renal artery for 20 min. Five minutes after drug administration, all rats except sham underwent 45 min of left renal ischemia followed by 24 h of reperfusion. Kidneys were harvested for histological and biochemical evaluation. Levels of TLRs, downstream signaling molecules and pro-inflammatory cytokines were determined by Western blot or immunohistochemistry. Hematoxylin and eosin (H&E) stained renal sections were used for histological grading of renal injury. Apoptotic cells were detected by TUNEL assay. Compared to the sham group, rats in the IR group showed higher renal levels of TLR-2, TLR-4, nuclear NF-kB p65, phosphorylated ASK1, phosphorylated TRAF2, IL-1b, IL-6, IL-18 and TNF-a (p50.05), and exhibited acute kidney injury (p50.05) and apoptosis (p50.05). Compared to the IR group, rats receiving PAG or HA showed significantly higher levels of TLR-2, TLR-4, nuclear NF-kB p65, phosphorylated ASK1, phosphorylated TRAF2, IL-1b, IL-6, IL-18 and TNF-a (p50.01), more severe acute kidney injury (p50.05) and increased apoptosis (p50.01). Thus, inflammatory response and apoptosis mediated by TLRs are involved in renal IRI. Inhibition of endogenous H 2 S significantly activated inflammatory response and apoptosis, and thus promoted renal IRI.

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Hydrogen sulfide protects rat lung from ischemia–reperfusion injury

Cited by 126 publications

References 26 publications

Cystathionine γ-Lyase Protects against Renal Ischemia/Reperfusion by Modulating Oxidative Stress

Cystathionine γ-Lyase Protects against Renal Ischemia/Reperfusion by Modulating Oxidative Stress

Hydrogen sulfide treatment improves long-term renal dysfunction resulting from prolonged warm renal ischemia-reperfusion injury

Impact of endogenous hydrogen sulfide on toll-like receptor pathway in renal ischemia/reperfusion injury in rats

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