Dynamic change of hydrogen sulfide during global cerebral ischemia–reperfusion and its effect in rats

Caili, Ren; Du, Aihua; Li, Dongliang; Sui, Jinwen; Mayhan, William G.; Zhao, Heng

doi:10.1016/j.brainres.2010.05.017

Cited by 74 publications

(65 citation statements)

References 47 publications

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“…In normal hippocampus, acid-labile sulfur could not be changed by using low concentration (100 lmol/kg) exogenous H 2 S; however, it will be enhanced in 2VO hippocampus. The results are in line with previous reports [27,50]. A previous research suggested that brain ischemia induced a decrease in the enzyme activity of CBS [50].…”

Section: Discussionsupporting

confidence: 95%

Protective Effects of Exogenous Hydrogen Sulfide on Neurons of Hippocampus in a Rat Model of Brain Ischemia

Wang

Xie

et al. 2011

Neurochem Res

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Many studies have demonstrated the cytoprotective effects of hydrogen sulfide (H(2)S) in vitro and/or in vivo ischemic injury. The aim of the current study was to investigate whether exogenous H(2)S attenuates the neuronal injury induced by brain ischemia. As an H(2)S donor, sodium hydrosulfide (NaHS) was administered intraperitoneally (5.6 mg/kg/day, i.p.). The effects of exogenous H(2)S on neurons of ischemic hippocampus were examined by using measurement of behavior, electrophysiology, morphology and immunohistochemical staining, respectively. Our results showed that exogenous H(2)S significantly improved spatial learning and memory deficits induced by brain ischemia (P < 0.01). Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. The results suggest a protective effect and therapeutic potential of H(2)S in the treatment of brain ischemia.

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Section: Discussionsupporting

confidence: 95%

Protective Effects of Exogenous Hydrogen Sulfide on Neurons of Hippocampus in a Rat Model of Brain Ischemia

Wang

Xie

et al. 2011

Neurochem Res

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“…found that exogenous H 2 S aggravated acute focal cerebral ischemic injury. This contradiction is attributed to the different dose of donor of H 2 S, which lower rather than higher concentration of exogenous H 2 S might offer a protection against the neuronal injury [31,32].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Zhu

Feng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hydrogen sulfide (H₂S) can decrease blood-brain barrier (BBB) permeability after cardiac arrest (CA) and resuscitation; however, the underlying mechanisms are not understood clearly. Methods: We investigated the effects of inhalation of H₂S on CA and resuscitation in a rat model of CA. We used Evans blue to detect the integrity of BBB and Western blot to assess the activation of protein kinase c (PKC) isozymes and the expression of Claudin-5, Occludin, and ZO-1. Neurological deficit scales and the 14-days survival rate were measured. Results: We determined that inhalation of 40 p.p.m or 80 p.p.m H₂S significantly decreased brain water content and Evans blue leakage, ameliorated neurologic deficit scale and improved 14-days survival rate. H₂S inhibited the activation of PKC-α, β I, β II and δ, impelled the activation of PKC-ε, and increased the expression of Claudin-5, Occludin and ZO-1. Conclusions: H₂S improved the integrity of BBB, mitigated brain edema; improved neurological outcome and 14-days survival rate in rats after CA and resuscitation. The beneficial effects of H₂S may be associated with inhibiting the activation of PKC-α, β I, β II and δ, promoting the activation of PKC-ε, and increasing the expression of Claudin-5, Occludin and ZO-1.

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“…H 2 S, which has been known for decades as a toxic gas, is currently recognized as a gaseous physiological molecule (1,11,42,48). Recent studies have demonstrated that H 2 S performs a cytoprotective role in a variety of organs, including the heart, brain, intestine, and kidney, against ischemia/reperfusion (I/ R) injury (5,41,49). Thus, it is possible that Msrs may be involved in the regulation of the trans-sulfuration pathway and the production of H 2 S.…”

mentioning

confidence: 99%

Protective Role of Methionine Sulfoxide Reductase A Against Ischemia/Reperfusion Injury in Mouse Kidney and Its Involvement in the Regulation of Trans-Sulfuration Pathway

Kim

Choi

Jung

et al. 2013

Antioxidants & Redox Signaling

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Aims: Methionine sulfoxide reductase A (MsrA) and methionine metabolism are associated with oxidative stress, a principal cause of ischemia/reperfusion (I/R) injury. Herein, we investigated the protective role of MsrA against kidney I/R injury and the involvement of MsrA in methionine metabolism and the transsulfuration pathway during I/R. Results: We found that MsrA gene-deleted mice (MsrA -/ -) were more susceptible to kidney I/R injury than wild-type mice (MsrA +/+ ). Deletion of MsrA enhanced renal functional and morphological impairments, congestion, inflammatory responses, and oxidative stress under I/R conditions. Concentrations of homocysteine and H 2 S in the plasma of control MsrA -/ -mice were significantly lower than those in control MsrA +/+ mice. I/R reduced the levels of homocysteine and H 2 S in both MsrA +/+ and MsrA -/ -mice, and these reductions were significantly more profound in MsrA -/ -than in MsrA +/+ mice. I/R reduced the expression and activities of cystathionine-b-synthase (CBS) and cystathionine-c-lyase (CSE), both of which are H 2 S-producing enzymes, in the kidneys. These reductions were more profound in the MsrA -/ -mice than in the MsrA +/+ mice. Innovation: The data provided herein constitute the first in vivo evidence for the involvement of MsrA in regulating methionine metabolism and the trans-sulfuration pathway under normal and I/R conditions. Conclusion: Our data demonstrate that MsrA protects the kidney against I/R injury, and that this protection is associated with reduced oxidative stress and inflammatory responses. The data indicate that MsrA regulates H 2 S production during I/R by modulating the expression and activity of the CBS and CSE enzymes.

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Dynamic change of hydrogen sulfide during global cerebral ischemia–reperfusion and its effect in rats

Cited by 74 publications

References 47 publications

Protective Effects of Exogenous Hydrogen Sulfide on Neurons of Hippocampus in a Rat Model of Brain Ischemia

Protective Effects of Exogenous Hydrogen Sulfide on Neurons of Hippocampus in a Rat Model of Brain Ischemia

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Protective Role of Methionine Sulfoxide Reductase A Against Ischemia/Reperfusion Injury in Mouse Kidney and Its Involvement in the Regulation of Trans-Sulfuration Pathway

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