Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

Zhang, Bing; Cheng, Long; Chi, Meng; Deng, Lin; Pan, Hong; Yao, Xuan; Wang, Guonian

doi:10.1016/j.brainres.2015.07.001

Cited by 38 publications

(20 citation statements)

References 39 publications

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“…or 80 p.p.m. H 2 S. The present findings, in conjunction with these previously published data [17,[43][44][45], suggest that PKC is involved in the protective effect of H 2 S against CA and resuscitation.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 89%

“…Furthermore, it was confirmed that H 2 S reduced myocardium infarct size by activating PKC-ε and protecting the heart against ischemic/reperfusion injury [44]. In addition, Wei et al [45]. also found that exogenous H 2 S activated PKC and down-regulated the expression of AQP4 in a local cerebral ischemia model.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 85%

“…As a third essential gas molecule, several studies have confirmed that H 2 S could regulate the activation and expression of PKC [18,[43][44][45]. Tiong et al [17].…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 98%

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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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Section: Cellular Physiology and Biochemistrysupporting

confidence: 89%

Section: Cellular Physiology and Biochemistrymentioning

confidence: 85%

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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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“…These results lend credence to the notion that H 2 S provide neuroprotection in ischemic brain tissue. Wei et al23 revealed that 40 ppm and 80 ppm H 2 S inhalation reduced brain edema and infarct volume through inhibiting the expression of AQP-4 via activating protein kinase C (PKC) in MCAO rats. Co-administration of two H 2 S donors, 5-(4-hydroxyphenyl)-3H-1,2-dithiocyclopentene-3-thione (ADT-OH) and sodium hydrosulfide (NaHS) with tPA attenuated hemorrhagic transformation following MCAO in mice 24.…”

Section: Oxygenmentioning

confidence: 99%

Medical gases for stroke therapy: summary of progress 2015–2016

et al. 2017

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Stroke is a cerebrovascular disease with high mortality and morbidity. Despite extensive research, there are only a very limited number of therapeutic approaches suitable for treatment of stroke patients as yet. Mounting evidence has demonstrated that such gases as oxygen, hydrogen and hydrogen sulfide are able to provide neuroprotection after stroke. In this paper, we will focus on the recent two years’ progress in the development of gas therapies of stroke and in understanding the molecular mechanisms underlying protection induced by medical gases. We will also discuss the advantages and challenges of these approaches and provide information for future study.

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“…It was reported that AQP4 was down-regulated by activating protein kinase C (PKC) pathway by hydrogen sulfide or melatonin after MCAO, suggesting PKC pathway is essential for AQP4 down-regulation [56,57]. Mitogen-activated protein kinase (MAPK) pathways include three main members: extracellular signal-regulated kinase (ERK), C-Jun amino-terminal kinase (JNK) and p38-MAPK.…”

Section: Cerebral Ischemiamentioning

confidence: 99%

Aquaporin-4 and Cerebrovascular Diseases

Chu

Huang

Ding

et al. 2016

IJMS

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Cerebrovascular diseases are conditions caused by problems with brain vasculature, which have a high morbidity and mortality. Aquaporin-4 (AQP4) is the most abundant water channel in the brain and crucial for the formation and resolution of brain edema. Considering brain edema is an important pathophysiological change after stoke, AQP4 is destined to have close relation with cerebrovascular diseases. However, this relation is not limited to brain edema due to other biological effects elicited by AQP4. Till now, multiple studies have investigated roles of AQP4 in cerebrovascular diseases. This review focuses on expression of AQP4 and the effects of AQP4 on brain edema and neural cells injuries in cerebrovascular diseases including cerebral ischemia, intracerebral hemorrhage and subarachnoid hemorrhage. In the current review, we pay more attention to the studies of recent years directly from cerebrovascular diseases animal models or patients, especially those using AQP4 gene knockout mice. This review also elucidates the potential of AQP4as an excellent therapeutic target.

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Hydrogen sulfide induces neuroprotection against experimental stroke in rats by down-regulation of AQP4 via activating PKC

Cited by 38 publications

References 39 publications

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

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

Medical gases for stroke therapy: summary of progress 2015–2016

Aquaporin-4 and Cerebrovascular Diseases

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