Sevoflurane postconditioning involves an up-regulation of HIF-1α and HO-1 expression via PI3K/Akt pathway in a rat model of focal cerebral ischemia

Zhi, Yong; Guo, Qulian; Xia, Pingping; Wang, Na; Wang, E.; Yuan, Yajing

doi:10.1016/j.brainres.2012.04.050

Cited by 85 publications

(67 citation statements)

References 37 publications

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“…Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. Recently, our laboratory has already demonstrated that sevoflurane postconditioning could alleviate ischemic reperfusion injury in the brain (11,28). However, the mechanism of sevoflurane protective effect on cerebral ischemia has not been well investigated.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the concept of postconditioning through modulation of reperfusion rather than ischemia has been proposed. Previous studies have suggested that the effect of sevoflurane to protect organs from ischemia-reperfusion injury and neuron death by administration immediately at the onset of reperfusion may be attributed to sevoflurane's antioxidant and free radical scavenging actions (10,11).…”

mentioning

confidence: 99%

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Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

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Background: Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. The purpose of this study was to investigate the effect of sevoflurane postconditioning on endogenous antioxidant status and spatial learning and memory ability after cardiac arrest (CA) and the potential underlying mechanisms. Methods: A rat model of CA was established by delivering an alternating current between the esophagus and chest wall to induce ventricular fibrillation. Animals were randomly divided into three groups: sham group (no CA), CA group, and CA + sevoflurane postconditioning (CA + SE) group. Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 60 min after resuscitation. The spatial learning and memory ability of rats was measured by the Morris water maze. The antioxidant enzymes activities were assessed at 4 hours, 1 day and 8 days after resuscitation. Moreover, the expressions of hippocampal proteins which could serve as memory enhancement biomarkers including growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD -95) and the transcription factor c-jun/activator protein-1 (AP-1), were detected at 8 days after resuscitation. Results: We found that CA significantly decreased the ability of spatial learning and memory in contrast to the sham controls. However, sevoflurane postconditioning significantly increased survival rate and antioxidant enzyme activities as well as ameliorated the spatial learning and memory deficits induced by CA. Furthermore, sevoflurane postconditioning regulated hippocampal memory enhancement proteins. Conclusions: Postconditioning with sevoflurane improved learning and memory deficits in a CA model possibly due to the reduction of oxidative stress and up-regulation of the memory enhancement biomarkers in hippocampus.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

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“…Однако необхо-димо отметить, что в данном исследовании не было изучено влияние изофлюрана при реперфузионном повреждении, поскольку была использована модель постоянной фокальной ишемии. В другом исследова-нии изучались механизмы нейропротективного влия-ния ПостК севофлюраном на модели фокальной ишемии-реперфузии головного мозга крысы, инду-цируемой 60-минутной окклюзией общих сонных артерий в комбинации с постоянной окклюзией средней мозговой артерии [19]. Применение ингаля-ционно 2,5% севофлюрана в течение 60 минут после моделирования постоянной окклюзии средней моз-говой артерии и завершения 60-минутной окклюзии общих сонных артерий с последующим 24-и 72-часо-вым реперфузионным периодом приводило к досто-верному уменьшению числа поврежденных нейронов в гистологических образцах ипсилатеральной обла-сти головного мозга, окрашенных по методу Ниссля, при сравнении с группой контроля [19].…”

Section: индуцируемый гипоксией фактор-1 (Hif-1)unclassified

“…В другом исследова-нии изучались механизмы нейропротективного влия-ния ПостК севофлюраном на модели фокальной ишемии-реперфузии головного мозга крысы, инду-цируемой 60-минутной окклюзией общих сонных артерий в комбинации с постоянной окклюзией средней мозговой артерии [19]. Применение ингаля-ционно 2,5% севофлюрана в течение 60 минут после моделирования постоянной окклюзии средней моз-говой артерии и завершения 60-минутной окклюзии общих сонных артерий с последующим 24-и 72-часо-вым реперфузионным периодом приводило к досто-верному уменьшению числа поврежденных нейронов в гистологических образцах ипсилатеральной обла-сти головного мозга, окрашенных по методу Ниссля, при сравнении с группой контроля [19]. Было уста-новлено, что ПостК севофлюраном приводит к досто-верному увеличению экспрессии мРНК генов HIF-1α и гемоксигеназы-1 (HO-1) в пенумбре к 6 и 24 часам реперфузионного периода при сравнении с группой без применения ПостК севофлюраном.…”

Section: индуцируемый гипоксией фактор-1 (Hif-1)unclassified

“…Уровень белков HIF-1α и HO-1 в группах с примене-нием и без применения ПостК севофлюраном был достоверно выше к 6, 24 и 72 часам реперфузионного периода, с максимальным увеличением при 24-часо-вой реперфузии при сравнении с ложнооперирован-ными животными. Однако статистически более высокий уровень экспрессии белков HIF-1α и HO-1 обнаруживался в группе с применением ПостК севофлюраном при длительности реперфузии 72 часа при сравнении с группой без ПостК [19]. Известно, что HO-1 превращает гем в биливердин, причем в результате этого превращения высвобождается железо и монооксид углерода [20][21][22].…”

Section: индуцируемый гипоксией фактор-1 (Hif-1)unclassified

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The Role of Hypoxia-Induced Factor-1 (Hif-1) in Cytoprotection Effect in Ischemic and Pharmacologic Postconditioning

Shcherbak¹,

Галагудза²,

Шляхто³

2015

Ross. kardiol. ž.

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В обзоре проанализированы результаты экспериментальных исследований, направленных на изучение влияния ишемического и фармакологического посткондиционирования печени, головного мозга, миокарда и скелетной мышцы на экспрессию и активность индуцируемого гипоксией фактора-1α (HIF-1α) у различных видов лабораторных животных. , Shlyakhto E. V. Российский 1,2The review concerns on the experimental studies results of the influence of ischemic and pharmacological post conditioning of the liver, brain, myocardium and scelet muscle on the expression and activity of the hypoxia-induced factor-1α (HIF-1α) in various types of lab animals. Russ

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Hydrogen sulfide restores sevoflurane postconditioning mediated cardioprotection in diabetic rats: Role of SIRT1/Nrf2 signaling‐modulated mitochondrial dysfunction and oxidative stress

Zhang

Cai

Zhang

et al. 2020

Journal Cellular Physiology

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Diabetic hearts are vulnerable to myocardial ischemia/reperfusion injury (IRI), but are insensitive to sevoflurane postconditioning (SPC), activating peroxiredoxins that confer cardioprotection. Previous studies have demonstrated that hydrogen sulfide (H2S) can suppress oxidative stress of diabetic rats through increasing the expression of silent information regulator factor 2‐related enzyme 1 (SIRT1), but whether cardioprotection by SPC can be restored afterward remains unclear. Diabetic rat was subjected to IRI (30 min of ischemia followed by 120 min reperfusion). Postconditioning treatment with sevoflurane was administered for 15 min upon the onset of reperfusion. The diabetic rats were treated with GYY4137 (H2S donor) 5 days before the experiment. Myocardial infarct size, mitochondrial structure and function, ATP content, activities of complex I‐IV, marker of oxidative stress, SIRT1, nuclear factor E2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), and NADPH Oxidase‐2 (Nox‐2) protein expression were detected after reperfusion, and cardiac function was evaluated by echocardiography at 24 h after reperfusion. After H2S activated SIRT1 in the impaired myocardium of diabetic rats, SPC significantly upregulated the expression of Nrf2 and its downstream mediator HO‐1, thus reduced the expression of Nox‐2. In addition, H2S remarkably increased cytoplasmic and nuclear SIRT1 which was further enhanced by SPC. Furthermore, H2S combined with SPC reduced the production of reactive oxygen species, increased the content of ATP, and maintained mitochondrial enzyme activity. Finally, myocardial infarct size and myocardium damage were decreased, and cardiac function was improved. Taken together, our study proved that H2S could restore SPC‐induced cardioprotection in diabetic rats by enhancing and promoting SIRT1/Nrf2 signaling pathway mediated mitochondrial dysfunction and oxidative stress.

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Sevoflurane postconditioning involves an up-regulation of HIF-1α and HO-1 expression via PI3K/Akt pathway in a rat model of focal cerebral ischemia

Cited by 85 publications

References 37 publications

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

The Role of Hypoxia-Induced Factor-1 (Hif-1) in Cytoprotection Effect in Ischemic and Pharmacologic Postconditioning

Hydrogen sulfide restores sevoflurane postconditioning mediated cardioprotection in diabetic rats: Role of SIRT1/Nrf2 signaling‐modulated mitochondrial dysfunction and oxidative stress

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