Biologic Effect of Hydrogen Sulfide and Its Role in Traumatic Brain Injury

Zhang, Jiaxin; Zhang, Shaoyi; Shan, Haiyan; Zhang, Mingyang

doi:10.1155/2020/7301615

Cited by 25 publications

(27 citation statements)

References 77 publications

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“…H 2 S has been described as a potent antioxidant in several organ systems [ 48 , 49 , 50 ]. In a murine model of acute lung injury induced by LPS-induced endotoxemia, the H 2 S donor GYY 4137 attenuated the LPS-induced decrease in the antioxidative biomarkers catalase and SOD and the total antioxidant capacity (T-AOC) [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Inhalative as well as Intravenous Administration of H2S Provides Neuroprotection after Ischemia and Reperfusion Injury in the Rats’ Retina

Scheid

Goeller

Baar

et al. 2022

IJMS

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Background: Neuronal ischemia-reperfusion injury (IRI), such as it can occur in glaucoma or strokes, is associated with neuronal cell death and irreversible loss of function of the affected tissue. Hydrogen sulfide (H2S) is considered a potentially neuroprotective substance, but the most effective route of application and the underlying mechanism remain to be determined. Methods: Ischemia-reperfusion injury was induced in rats by a temporary increase in intraocular pressure (1 h). H2S was then applied by inhalation (80 ppm at 0, 1.5, and 3 h after reperfusion) or by intravenous administration of the slow-releasing H2S donor GYY 4137. After 24 h, the retinas were harvested for Western blotting, qPCR, and immunohistochemical staining. Retinal ganglion cell survival was evaluated 7 days after ischemia. Results: Both inhalative and intravenously delivered H2S reduced retinal ganglion cell death with a better result from inhalative application. H2S inhalation for 1.5 h, as well as GYY 4137 treatment, increased p38 phosphorylation. Both forms of application enhanced the extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation, and inhalation showed a significant increase at all three time points. H2S treatment also reduced apoptotic and inflammatory markers, such as caspase-3, intracellular adhesion molecule 1 (ICAM-1), vascular endothelial growth factor (VEGF), and inducible nitric oxide synthase (iNOS). The protective effect of H2S was partly abolished by the ERK1/2 inhibitor PD98059. Inhalative H2S also reduced the heat shock response including heme oxygenase (HO-1) and heat shock protein 70 (HSP-70) and the expression of radical scavengers such as superoxide dismutases SOD1, SOD2) and catalase). Conclusion: Hydrogen sulfide acts, at least in part, via the mitogen-activated protein kinase (MAPK) ERK1/2 to reduce apoptosis and inflammation. Both inhalative H2S and intravenous GYY 4137 administrations can improve neuronal cell survival.

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Section: Discussionmentioning

confidence: 99%

Inhalative as well as Intravenous Administration of H2S Provides Neuroprotection after Ischemia and Reperfusion Injury in the Rats’ Retina

Scheid

Goeller

Baar

et al. 2022

IJMS

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“…H 2 S can bind to hemoglobin to form sulfhemoglobin, which may be one of the storage forms of H 2 S in vivo 30 . In addition, the recognized form of H 2 S storage in the body is the acid‐labile sulfur pool such as iron‐sulfur cluster‐containing proteins, and reductant‐labile sulfane sulfur pool, which include hydrodisulfides/persulfides 45,46 …”

Section: Storage Of H2smentioning

confidence: 99%

“…30 In addition, the recognized form of H 2 S storage in the body is the acid-labile sulfur pool such as iron-sulfur cluster-containing proteins, and reductant-labile sulfane sulfur pool, which include hydrodisulfides/persulfides. 45,46…”

Section: S Tor Ag E Of H 2 Smentioning

confidence: 99%

“…56 Moreover, another study on TBI mice demonstrated that the protective effect of H 2 S in TBI may be associated with the regulation of apoptosis and autophagy. 57 In 2020, a review by Zhang et al 46 further summarized the potential role of H 2 S in TBI. Their work suggested that H 2 S could reduce secondary brain injury after TBI via antioxidation and antiinflammatory effects, and by regulating cell death signaling and alleviating cerebral vasospasm and brain edema.…”

Section: Appli C Ati On Of H 2 S In Cn S Dise a Se Smentioning

confidence: 99%

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Role of hydrogen sulfide in subarachnoid hemorrhage

Wang

Liu

et al. 2022

CNS Neurosci Ther

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Subarachnoid hemorrhage (SAH) is a common acute and severe disease worldwide, which imposes a heavy burden on families and society. However, the current therapeutic strategies for SAH are unsatisfactory. Hydrogen sulfide (H2S), as the third gas signaling molecule after carbon monoxide and nitric oxide, has been widely studied recently. There is growing evidence that H2S has a promising future in the treatment of central nervous system diseases. In this review, we focus on the effects of H2S in experimental SAH and elucidate the underlying mechanisms. We demonstrate that H2S has neuroprotective effects and significantly reduces secondary damage caused by SAH via antioxidant, antiinflammatory, and antiapoptosis mechanisms, and by alleviating cerebral edema and vasospasm. Based on these findings, we believe that H2S has great potential in the treatment of SAH and warrants further study to promote its early clinical application.

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“…Hydrogen sulfide (H 2 S) is a gaseous neurotransmitter that has been synthesized endogenously by cystathionine-γ-lyase and cystathionine-β-synthase 13 . Studies have shown the function of physiological and pathophysiological roles of H 2 S in the brain including traumatic brain injury 14 , 15 . Furthermore, other studies have pointed out the close interrelationship between H 2 S, neuroinflammation and Nrf2 16 , 17 .…”

Section: Introductionmentioning

confidence: 99%

Octreotide-mediated neurofunctional recovery in rats following traumatic brain injury. Role of H2S, Nrf2 and TNF-α

Zhou

Cao²,

Feng

et al. 2021

Acta Cir. Bras.

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Purpose: To explore the role and mechanisms of octreotide in neurofunctional recovery in the traumatic brain injury (TBI) model. Methods: Rats were subjected to midline incision followed by TBI in the prefrontal cortex region. After 72 hours, the behavioural and neurological deficits tests were performed, which included memory testing on Morris water maze for 5 days. Octreotide (15 and 30 mg/kg i.p. ) was administered 30 minutes before subjecting to TBI, and its administration was continued for three days. Results: In TBI-subjected rats, administration of octreotide restored on day 4 escape latency time (ELT) and increased the time spent in the target quadrant (TSTQ) on day 5, suggesting the improvement in learning and memory. It also increased the expression of H 2 S, Nrf2, and cystathionine-γ-lyase (CSE) in the prefrontal cortex, without any significant effect on cystathionine-β-synthase. Octreotide also decreased the TNF-α levels and neurological severity score. However, co-administration of CSE inhibitor (D,L-propargylglycine) abolished octreotide-mediated neurofunctional recovery, decreased the levels of H 2 S and Nrf2 and increased the levels of TNF-α. Conclusions: Octreotide improved the neurological functions in TBI-subjected rats, which may be due to up-regulation of H 2 S biosynthetic enzyme (CSE), levels of H 2 S and Nrf2 and down-regulation of neuroinflammation.

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Biologic Effect of Hydrogen Sulfide and Its Role in Traumatic Brain Injury

Cited by 25 publications

References 77 publications

Inhalative as well as Intravenous Administration of H2S Provides Neuroprotection after Ischemia and Reperfusion Injury in the Rats’ Retina

Inhalative as well as Intravenous Administration of H2S Provides Neuroprotection after Ischemia and Reperfusion Injury in the Rats’ Retina

Role of hydrogen sulfide in subarachnoid hemorrhage

Octreotide-mediated neurofunctional recovery in rats following traumatic brain injury. Role of H2S, Nrf2 and TNF-α

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