Sevoflurane preconditioning improves mitochondrial function and long-term neurologic sequelae after transient cerebral ischemia

Ye, Ruidong; Yang, Qianzi; Kong, Xiangdong; Li, Nanlin; Zhang, Yunxia; Han, Junliang; Xiong, Li; Liu, Xinfeng; Zhao, Gang

doi:10.1097/ccm.0b013e318258fb90

Cited by 58 publications

(30 citation statements)

References 44 publications

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“…Western blot analysis was performed as described previously (46,47). Briefly, total cell lysates were extracted by using RIPA lysis buffer (Cell Signaling Technology) containing 1 mM PMSF and 1ϫ phosphatase inhibitors (Roche Applied Science) on ice.…”

Section: Methodsmentioning

confidence: 99%

Caveolin-1 is a checkpoint regulator in hypoxia-induced astrocyte apoptosis via Ras/Raf/ERK pathway

Wang

Wen

et al. 2016

American Journal of Physiology-Cell Physiology

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Astrocytes, the most numerous cells in the human brain, play a central role in the metabolic homeostasis following hypoxic injury. Caveolin-1 (Cav-1), a transmembrane scaffolding protein, has been shown to converge prosurvival signaling in the central nerve system. The present study aimed to investigate the role of Cav-1 in the hypoxia-induced astrocyte injury. We also examined how Cav-1 alleviates apoptotic astrocyte death. To this end, primary astrocytes were exposed to oxygen-glucose deprivation (OGD) for 6 h and a subsequent 24-h reoxygenation to mimic hypoxic injury. OGD significantly reduced Cav-1 expression. Downregulation of Cav-1 using Cav-1 small interfering RNA dramatically worsened astrocyte cell damage and impaired cellular glutamate uptake after OGD, whereas overexpression of Cav-1 with Cav-1 scaffolding domain peptide attenuated OGD-induced cell apoptosis. Mechanistically, the expressions of Ras-GTP, phospho-Raf, and phospho-ERK were sequestered in Cav-1 small interfering RNA-treated astrocytes, yet were stimulated after supplementation with caveolin peptide. MEK/ERK inhibitor U0126 remarkably blocked the Cav-1-induced counteraction against apoptosis following hypoxia, indicating Ras/Raf/ERK pathway is required for the Cav-1's prosurvival role. Together, these findings support Cav-1 as a checkpoint for the in hypoxia-induced astrocyte apoptosis and warrant further studies targeting Cav-1 to treat hypoxic-ischemic brain injury.

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Section: Methodsmentioning

confidence: 99%

Caveolin-1 is a checkpoint regulator in hypoxia-induced astrocyte apoptosis via Ras/Raf/ERK pathway

Wang

Wen

et al. 2016

American Journal of Physiology-Cell Physiology

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“…In contrast, there was no benefit from an 8 h pre-ischemic exposure to either halothane or propofol. That a brief anesthetic exposure improves the outcome of a cerebral ischemic insult has been extended to isoflurane [131], sevoflurane [132], dexmedetomidine [133] and chloral hydrate [134], including long term (2-4 weeks) outcome [135, 136]. In contrast, alpha-chloralose may be devoid of this property [65], and ketamine may indeed block ischemic preconditioning mediated by activation of the NMDA receptor [137].…”

Section: Anesthetic Preconditioningmentioning

confidence: 99%

Anesthesia in Experimental Stroke Research

Hoffmann

Sheng

Ayata

et al. 2016

Transl. Stroke Res.

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Anesthetics have enabled major advances in development of experimental models of human stroke. Yet their profound pharmacologic effects on neural function can confound the interpretation of experimental stroke research. Anesthetics have drug and dose-specific effects on cerebral blood flow and metabolism, neurovascular coupling, autoregulation, ischemic depolarizations, excitotoxicity, inflammation, neural networks, and numerous molecular pathways relevant for stroke outcome. Both pre- and post-conditioning properties have been described. Anesthetics also modulate systemic arterial blood pressure, lung ventilation, and thermoregulation, all of which may interact with the ischemic insult as well as the therapeutic interventions. These confounds present a dilemma. Here, we provide an overview of the anesthetic mechanisms of action and molecular and physiologic effects on factors relevant to stroke outcomes that can guide the choice and optimization of the anesthetic regimen in experimental stroke.

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“…This sobering reality should not be misconstrued as evidence that neuroprotection or neurorestoration is unattainable in patients (Tymianski, 2010). On the contrary, an abundance of laboratory studies have defined and characterized the pathophysiology of ischemic brain injury and have provided scientifically irrefutable proof-of-principle that stroke restoration, in fact, is feasible with a variety of interventions (Sahota and Savitz, 2011; Ye et al, 2011, 2012). Moreover, the stroke community has accumulated ample experience, positive and negative, from those prior failures (Ye et al, 2013).…”

Section: Prospects and Conclusionmentioning

confidence: 99%

Cell based therapies for ischemic stroke: From basic science to bedside

Liu

Yan

et al. 2014

Progress in Neurobiology

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166

143

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Cell therapy is emerging as a viable therapy to restore neurological function after stroke. Many types of stem/progenitor cells from different sources have been explored for their feasibility and efficacy for the treatment of stroke. Transplanted cells not only have the potential to replace the lost circuitry, but also produce growth and trophic factors, or stimulate the release of such factors from host brain cells, thereby enhancing endogenous brain repair processes. Although stem/progenitor cells have shown a promising role in ischemic stroke in experimental studies as well as initial clinical pilot studies, cellular therapy is still at an early stage in humans. Many critical issues need to be addressed including the therapeutic time window, cell type selection, delivery route, and in vivo monitoring of their migration pattern. This review attempts to provide a comprehensive synopsis of preclinical evidence and clinical experience of various donor cell types, their restorative mechanisms, delivery routes, imaging strategies, future prospects and challenges for translating cell therapies as a neurorestorative regimen in clinical applications.

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Sevoflurane preconditioning improves mitochondrial function and long-term neurologic sequelae after transient cerebral ischemia

Abstract: Sevoflurane preconditioning protects mitochondria from cerebral ischemia/reperfusion injury and ameliorates long-term neurological deficits. Inhibition of mitochondrial permeability transition pore opening is a crucial step in mediating the neuroprotection of sevoflurane preconditioning.

Cited by 58 publications

References 44 publications

Caveolin-1 is a checkpoint regulator in hypoxia-induced astrocyte apoptosis via Ras/Raf/ERK pathway

Caveolin-1 is a checkpoint regulator in hypoxia-induced astrocyte apoptosis via Ras/Raf/ERK pathway

Anesthesia in Experimental Stroke Research

Cell based therapies for ischemic stroke: From basic science to bedside

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