Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway

Wang, Jun-Kuan; Lu, Yu; Zhang, Fengjiang; Yang, Ming; Yu, Jing; Yan, Min; Chen, Gao

doi:10.1016/j.brainres.2010.08.009

Cited by 94 publications

(61 citation statements)

References 47 publications

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“…Consistent with previous studies, MCAO resulted in an increased escape latency and path length relative to sham and unoperated animals in a watermaze spatial reference-memory task (Markgraf et al, 1992;Pavlichenko et al, 2008;Sadamoto et al, 1998;Shinoda et al, 1996;Smith et al, 1997;Wang et al, 2010;Xu et al, 2009;Yonemori et al, 1996;Yun et al, 2007;Zhang et al, 2010). However, from close scrutiny of the behavior of MCAO animals in the watermaze, the present study indicates that maintained focal ischemia within the MCA territory has little effect on the acquisition and retention of spatial reference memory.…”

Section: Discussionsupporting

confidence: 91%

“…Understanding these functional deficits is essential for development of future therapies. Many experimental studies have used watermaze tasks to better understand spatial learning and memory deficits after MCA occlusion (MCAO) and to assess potential future therapies (Hayase et al, 2009;Kawanishi et al, 2010;Markgraf et al, 1992;Noh et al, 2011;Pavlichenko et al, 2008;Sadamoto et al, 1998;Shinoda et al, 1996;Smith et al, 1997;Wang et al, 2010;Xu et al, 2009;Yonemori et al, 1996;Yun et al, 2007;Zhang et al, 2010). However, in rodent experimental stroke models, investigation of deficits in spatial memory using the Morris watermaze may be confounded by coexisting sensory and motor impairments.…”

Section: Introductionmentioning

confidence: 99%

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Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

Bingham

Martin

Macrae

et al. 2012

J Cereb Blood Flow Metab

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In rodent stroke models, investigation of deficits in spatial memory using the Morris watermaze may be confounded by coexisting sensory or motor impairments. To target memory specifically, we devised a watermaze protocol to minimize the impact of sensory and motor impairments in female Lister-hooded rats exposed to proximal electrocoagulation of the middle cerebral artery (MCAO). Rats were trained in a reference-memory task comprising 4 trials/day; trial 1 being a probe trial (platform absent for the first 60 seconds). Training ended once animals reached a strict criterion based on the probe-trial performance. Memory retention was tested 1, 7, and 28 days later. The MCAO did not affect the number of days to reach criterion during acquisition or the time spent in target quadrant during retention testing, compared with sham or unoperated rats. However, MCAO rats showed slightly poorer accuracy in crossing the platform location and increased thigmotactic swimming compared with controls. Our results show that spatial memory deficits are minimal in this rodent stroke model, and suggest that previously published watermaze impairments are attributable to sensory and motor deficits but not memory deficits. We recommend using probe trials and training to a predetermined performance criterion in future studies assessing watermaze memory deficits in rodent stroke models.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

Bingham

Martin

Macrae

et al. 2012

J Cereb Blood Flow Metab

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“…Moreover, higenamine-induced HO-1 induction was significantly reduced by LY 294002, indicating that induction of HO-1 by higenamine involves in PI3K/Akt signal. Indeed, the neuroprotective role of the PI3K/Akt pathway in cerebral ischemia has been widely studied [28,29]. Besides PI3K/Akt signal, we could not rule out the possibility the involvement of protein kinase A (PKA) for induction of HO-1 by higenamine.…”

Section: Discussionmentioning

confidence: 90%

“…Because hypoxia induces cellular injury through an increase in the mitochondrial generation of ROS in many cells [4], and 20 mU/ml GOX was sufficient to generate ROS [20], where the generation of sustained and continual release of H 2 O 2 can give rise to oxidative stress as in hypoxia [32]. In addition, PI3K/Akt pathway that has a relevant role in the inhibition of apoptosis [20,21,28,29], Fig. 5 Higenamine inhibits ROS-induced apoptosis with PI3K-sensitive manner.…”

Section: Discussionmentioning

confidence: 98%

Higenamine reduces HMGB1 during hypoxia-induced brain injury by induction of heme oxygenase-1 through PI3K/Akt/Nrf-2 signal pathways

Kim

Park

et al. 2011

Apoptosis

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Growing lines of evidence suggests that high mobility group box-1 (HMGB1) plays an important role for promoting inflammation and apoptosis in brain ischemia. Previously, we demonstrated that inducers of heme oxygenase-1 (HO-1) significantly reduce HMGB1 release in inflammatory conditions in vitro and in vivo. Thus, we tested our hypothesis that higenamine protects brain injury by inhibition of middle cerebral artery occlusion (MCAO)-mediated HMGB1 release in vivo, and glucose/glucose oxidase (GOX)-induced apoptosis in C6 cells in vitro due to HO-1 induction. Higenamine increased HO-1 expression in C6 cells in both hypoxia and normoxia, in which the former was much more significant than the latter. Higenamine increased Nrf-2 luciferase activity, translocated Nrf-2 to nucleus, and increased phosphorylation of Akt in C6 cells. Consistent with this, LY 294002, a PI3K inhibitor, inhibited HO-1 induction by higenamine and apoptosis induced by glucose/GOX in C6 cells was prevented by higenamine, which effect was reversed by LY 294002. Importantly, administration of higenamine (i.p) significantly reduced brain infarct size, mortality rate, MPO activity and tissue expression of HMGB1 in MCAO rats. In addition, recombinant high mobility group box 1 induced apoptosis in C6 cells by increasing ratio of Bax/bcl-2 and cleaved caspase c, which was inhibited by higenamine, and all of these effects were reversed by co-treatment with ZnPPIX. Therefore, we conclude that higenamine, at least in part, protects brain cells against hypoxic damages by up-regulation of HO-1. Thus, higenamine may be beneficial for the use of ischemic injuries such as stroke.

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“…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%

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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Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway

Cited by 94 publications

References 47 publications

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

Higenamine reduces HMGB1 during hypoxia-induced brain injury by induction of heme oxygenase-1 through PI3K/Akt/Nrf-2 signal pathways

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

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