Hydrogen sulfide renal protective effects: possible link between hydrogen sulfide and endogenous carbon monoxide in a rat model of renal injury

Aziz, Neven Makram; Elbassuoni, Eman; Kamel, Maha Yehia; Ahmed, Sabreen Mahmoud

doi:10.1007/s12192-019-01055-2

Cited by 24 publications

(19 citation statements)

References 37 publications

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“…Although this pathway is not fully understood, these authors have also suggested that NOS isoforms can accelerate chronic kidney damage depending on their concentration and site; however, further studies should be conducted to help better understanding this mechanism. Similar pattern was also observed for renal injury model induced by gentamicin and treated with exogenous H 2 S donor, in the presence and absence of CO synthesis inhibitor [ 124 ]. The treatment was capable of reducing renal NO levels and iNOS isoform overexpression, as well as of preventing eNOS degradation and inducing its phosphorylation.…”

Section: Crosstalk Between Gasotransmitters: Possible Mechanisms Of Isupporting

confidence: 80%

“…The treatment was capable of reducing renal NO levels and iNOS isoform overexpression, as well as of preventing eNOS degradation and inducing its phosphorylation. Interestingly, this crosstalk was capable of minimizing toxic peroxynitrite formation and, at the same time, it promoted ideal NO release enough to enable blood vessel dilation [ 124 ]. Moreover, the authors have shown that effects of H 2 S were minimized in the presence of CO inhibitor, suggesting that all three gasotransmitters presented important and linked pathways in the biological system [ 124 ].…”

Section: Crosstalk Between Gasotransmitters: Possible Mechanisms Of Imentioning

confidence: 99%

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H2S- and NO-releasing gasotransmitter platform: A crosstalk signaling pathway in the treatment of acute kidney injury

Pieretti

Junho

Carneiro‐Ramos

et al. 2020

Pharmacological Research

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Section: Crosstalk Between Gasotransmitters: Possible Mechanisms Of Isupporting

confidence: 80%

Section: Crosstalk Between Gasotransmitters: Possible Mechanisms Of Imentioning

confidence: 99%

H2S- and NO-releasing gasotransmitter platform: A crosstalk signaling pathway in the treatment of acute kidney injury

Pieretti

Junho

Carneiro‐Ramos

et al. 2020

Pharmacological Research

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“…genes (Amorim et al 2015;Wang et al 2015;Bruchim et al 2019). Heme oxygenase (HO)-1, also known as HSP32, is a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin, and iron (Raffaele et al 2019;Aziz et al 2020). HO-1 expression prevents a pulmonary inflammatory response to hypoxia, cardiac ischemia/reperfusion injury, and polycystic kidney disease (Minamino et al 2001;Nath 2006;He et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Expression of heme oxygenase-1 in type II pneumocytes protects against heatstroke-induced lung damage

Tseng

Liu

Lin

et al. 2021

Cell Stress and Chaperones

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Heatstroke (HS) is an acute clinical disease characterized by abnormal hyperthermia and multi-organ dysfunction. Heme oxygenase (HO)-1, also called heat shock protein (HSP)32, is induced by hyperthermia and also plays protective roles in many lung disease models. Based on this phenomenon, we investigated the protective role of endogenous HO-1 in heatinduced lung damage in rats. Male Sprague-Dawley (SD) rats were separated into three groups: (a) normothermic sham, (b) HS, and (c) SnPP (inhibitor of HO-1) pretreatment rats. In the HS group, rats were killed at various time points (1, 3, 6, and 12 h after heat exposure) in order to analyze messenger ribonucleic acid (mRNA) and protein levels. Lung sections were examined for tissue damage and localization of HO-1 using immunofluorescence double labeling. We found that HS induced lung pathology (congested and thickened lung septa). The level of HO-1 mRNA was increased at 1 h, and the protein level peaked at 6 h after heat exposure. Pretreatment with SnPP (tin-protoporphyrin IX, 30 mg/kg, intraperitoneal injection for 1 h before heat exposure) aggravated the lung damage. Furthermore, we demonstrated HO-1 expression in lung type II pneumocytes. Our results suggest that endogenous HO-1 is protective against HS-induced lung damage. Induction of HO-1 may be a potential therapeutic strategy for treating heat-related diseases.

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“…In addition, recent in vivo studies reveal the nephroprotective effects of H 2 S on renal tissue through upregulation of antioxidant proteins and anti-inflammatory cytokines, as well as the expression of eNOS and iNOS via induction of the Nrf2/HO-1 pathway in renal injury [ 302 ] and in the spinal cord of rats [ 303 ]. Moreover, H 2 S could attenuate high glucose-induced myocardial injury in rat cardiomyocytes by suppressing the Wnt/β-catenin pathway and upregulating the expression of HO-1 and NQO1 [ 304 ].…”

Section: H 2 S Redox Signaling and Resiliencementioning

confidence: 99%

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

et al. 2020

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Emerging evidence indicates that the dysregulation of cellular redox homeostasis and chronic inflammatory processes are implicated in the pathogenesis of kidney and brain disorders. In this light, endogenous dipeptide carnosine (β-alanyl-L-histidine) and hydrogen sulfide (H2S) exert cytoprotective actions through the modulation of redox-dependent resilience pathways during oxidative stress and inflammation. Several recent studies have elucidated a functional crosstalk occurring between kidney and the brain. The pathophysiological link of this crosstalk is represented by oxidative stress and inflammatory processes which contribute to the high prevalence of neuropsychiatric disorders, cognitive impairment, and dementia during the natural history of chronic kidney disease. Herein, we provide an overview of the main pathophysiological mechanisms related to high levels of pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and neurotoxins, which play a critical role in the kidney–brain crosstalk. The present paper also explores the respective role of H2S and carnosine in the modulation of oxidative stress and inflammation in the kidney–brain axis. It suggests that these activities are likely mediated, at least in part, via hormetic processes, involving Nrf2 (Nuclear factor-like 2), Hsp 70 (heat shock protein 70), SIRT-1 (Sirtuin-1), Trx (Thioredoxin), and the glutathione system. Metabolic interactions at the kidney and brain axis level operate in controlling and reducing oxidant-induced inflammatory damage and therefore, can be a promising potential therapeutic target to reduce the severity of renal and brain injuries in humans.

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Hydrogen sulfide renal protective effects: possible link between hydrogen sulfide and endogenous carbon monoxide in a rat model of renal injury

Cited by 24 publications

References 37 publications

H2S- and NO-releasing gasotransmitter platform: A crosstalk signaling pathway in the treatment of acute kidney injury

H2S- and NO-releasing gasotransmitter platform: A crosstalk signaling pathway in the treatment of acute kidney injury

Expression of heme oxygenase-1 in type II pneumocytes protects against heatstroke-induced lung damage

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

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