Sevoflurane Postconditioning Ameliorates Oxygen–Glucose Deprivation—Reperfusion Injury in the Rat Hippocampus

Peng, Sheng; Kalikiri, Pramood; Mychaskiw, George; Zhang, Dengxin; Zhang, Yan; Liu, Gongjian; Wang, Guanglei; Shen, Zhiyun

doi:10.1111/j.1755-5949.2010.00193.x

Cited by 25 publications

(15 citation statements)

References 23 publications

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“…The neuronal cultures were then directly placed in an anaerobic incubator (Thermo, Waltham, MA, USA) containing 100% N 2 at 37°C. After 90 min in OGD, the cultures were removed from the anaerobic incubator, immediately washed three times with BSS before adding an equal volume of Neuorbasal medium/B27/glutamine/gentamycin and incubated in a standard cell incubator containing 5% CO 2 , 95% air balance, and 98% humidity at 37°C for 24 h. In the sevoflurane postconditioning protocols, neuronal cultures were exposed immediately in a Billups-Rothenburg chamber that was bubbled with 2% of sevoflurane in 95% air-5% CO 2 at 6 L/min for 7-8 min after OGD [20]. Then the chamber was kept tightly sealed for 1 h at 37°C and the concentrations of sevoflurane in exhaust gas from the chamber was confirmed by the Datex™ infrared analyzer (Capnomac, Helsinki, Finland).…”

Section: Ogd/r and Sevoflurane Post-conditioningmentioning

confidence: 99%

WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

Zhang

Xun

Sun

et al. 2015

Journal of the Neurological Sciences

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Section: Ogd/r and Sevoflurane Post-conditioningmentioning

confidence: 99%

WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

Zhang

Xun

Sun

et al. 2015

Journal of the Neurological Sciences

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“…However, less is known about the postconditioning effect of sevoflurane, a more recent procedure that has also shown to be an effective therapeutic strategy to reduce ischemia-induced damage in the brain and myocardium [30,31] and to attenuate LPS-induced response in experimental models in pulmonary cells [7,32]. These studies have shown that beneficial effects of sevoflurane on LPS-mediated damage involve a reduction of cell death, an attenuation of the inflammatory response and chemotactic mechanisms, as well as an increase in the expression of molecules that protect cells against injury such as the chaperone HSP-32.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, most of our results are also observed at 7% sevoflurane, indicating that its dosage might differentially affect cell types. For example, postconditioning with up to 6% sevoflurane has shown beneficial effects in hippocampal tissue [30]. …”

Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane postconditioning on cell death, inflammation and TLR expression in human endothelial cells exposed to LPS

et al. 2013

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BackgroundSevoflurane is an anesthetic agent which also participates in protective mechanisms in sepsis, likely due to anti-inflammatory properties. A key tissue in sepsis is the endothelium, which expresses TLR2 and TLR4 receptors, known regulators of inflammatory mechanisms and potential therapeutic targets for this pathology. In this context, we explored the effect of sevoflurane postconditioning in an in vitro sepsis model.MethodsPrimary cultures of human umbilical vein endothelial cells were used for two different experiments. In the first set, cultures were placed in an airtight incubation chamber and exposed to different concentrations of sevoflurane (0,1,3 or 7% vol,) for 1 hour. In the second set, lipopolysaccharide from Escherichia coli 0111:B4 (1 μg/mL) was added to culture medium for 3 hours and cells were subsequently exposed to sevoflurane (0,1,3 or 7% vol,) for 1 hour as explained before. In both cases, cell viability was measured by MTT and Trypan blue assays, TLR2 and TLR4 expression were analyzed by flow cytometry, and TNFα and IL-6 levels were quantified in cell culture media by an immunoassay immediately after exposure, at 6 and 24 hours.ResultsExposure to 3% sevoflurane decreased TLR2 at 24 hours and TLR4 at 6 and 24 hours (both p<0.05), whereas exposure to 7% decreased TLR4 expression at 6 hours (p<0.05). Both 3 and 7% sevoflurane decreased TNF-α and IL-6 levels at 24 hours (both p<0.05). In LPS-stimulated cultures, exposure to 3% sevoflurane was cytoprotective at 6 and 24 hours (p<0.05) compared with control, and decreased TLR2 and TLR4 expression at 24 hours (p<0.05); whereas 7% decreased TLR4 expression at 24 hours (p<0.05). Both 3% and 7% sevoflurane decreased TNF-α and IL-6 levels at 24 hours (both p<0.05).ConclusionsPostconditioning with the halogenated anesthetic agent sevoflurane after LPS stimulation shows a cytoprotective effect in an in vitro model, decreasing cell death and reducing TLR2 and TLR4 expression as well as levels of the inflammatory mediators TNF-α and IL-6 in human endothelial cells.

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“…The neuronal cultures were then directly placed in an anaerobic incubator (Thermo, Waltham, MA, USA) containing 100 % N 2 at 37°C. After 90 min in OGD, the cultures were removed from the anaerobic incubator, immediately washed three times with BSS before adding an equal volume of Neuorbasal medium/B27/glutamine/gentamycin and incubated in a standard cell incubator containing 5 % CO 2 , 95 % air balance, 98 % humidity at 37°C for 24 h. In the sevoflurane post-conditioning protocols, neuronal cultures were exposed immediately in a Billups-Rothenburg chamber that was bubbled with different concentrations of sevoflurane in 95 % air-5 % CO 2 at 6 L/min for 7-8 min after OGD [21]. Then the chamber was kept tightly sealed for 1 h at 37°C and the concentrations of sevoflurane in exhaust gas from the chamber was confirmed by the Datex TM infrared analyzer (Capnomac, Helsinki, Finland).…”

Section: Ogd/r and Sevoflurane Post-conditioningmentioning

confidence: 99%

Sevoflurane Post-conditioning Protects Primary Rat Cortical Neurons Against Oxygen–Glucose Deprivation/Resuscitation: Roles of Extracellular Signal-Regulated Kinase 1/2 and Bid, Bim, Puma

Zhang

Xun²,

Jiang³

2015

Neurochem Res

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Temporal post-conditioning to induce neuroprotection against brain ischemia-reperfusion injury insult is considered to be an effective intervention, but the exact mechanisms of sevoflurane post-conditioning are poorly understood. Extracellular signal-related kinases 1/2 (Erk1/2) play a pivotal role in the cell growth and proliferation. The essential axis of activator Bid, Bim, Puma (BH3s) and BAX, BAK in activating the mitochondrial death program might offer common ground for cell death signal. We hypothesized that, sevoflurane post-conditioning might inhibit the expression of Bid, Bim and Puma and is activated by phosphor-Erk1/2 to reduce neuronal death. To test this hypothesis, we exposed primary cultured cortical neurons to oxygen-glucose deprivation for 1 h and resuscitation for 24 h (OGD/R). The assays of MTT, propidium iodide uptake, JC-1 fluorescence and western blot demonstrated that OGD/R exposure reduced cell viability, increased cell death, decreased mitochondrial membrane potential and the expressions of Bid, Bim, and Puma. Inhibition of Erk1/2 phosphorylation could partially attenuate 2 % of sevoflurane post-conditioning mediated increase in neuronal viability and mitochondrial membrane potential, and also a decrease in cell death and expression of Bid, Bim and Puma after OGD/R treatment. The results demonstrated that, the protection of sevoflurane post-conditioning markedly reducing death of cortical neurons exposed to OGD/R could be correlated with down-regulation of Bid, Bim and Puma expression mediated by phosphorylation/activation of Erk1/2.

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Sevoflurane Postconditioning Ameliorates Oxygen–Glucose Deprivation—Reperfusion Injury in the Rat Hippocampus

Abstract: Postconditioning with sevoflurane reduces neuronal damage after OGD-reperfusion injury in the CA1 area of rat hippocampus, in vitro.

Cited by 25 publications

References 23 publications

WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

Effects of sevoflurane postconditioning on cell death, inflammation and TLR expression in human endothelial cells exposed to LPS

Sevoflurane Post-conditioning Protects Primary Rat Cortical Neurons Against Oxygen–Glucose Deprivation/Resuscitation: Roles of Extracellular Signal-Regulated Kinase 1/2 and Bid, Bim, Puma

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