Isoflurane post-conditioning protects primary cultures of cortical neurons against oxygen and glucose deprivation injury via upregulation of Slit2/Robo1

Zhao, Xiao Chun; Zhang, Li Min; Li, Qiang; Tong, Dong Yi; Fan, Long; An, Ping; Wu, Xiu Ying; Chen, Wei Min; Zhao, Ping; Wang, Jian

doi:10.1016/j.brainres.2013.08.036

Cited by 15 publications

(12 citation statements)

References 34 publications

(34 reference statements)

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“…Isoflurane, however, appears to have protective properties as well. Survival of cortical neurons subjected to transient oxygen-glucose deprivation has been found to improve with isoflurane postconditioning [20]. Moreover, there appears to be reduced brain damage in mice exposed to isoflurane before or after ischemic injury [21,22] or in rats who received isoflurane after induction of germinal matrix hemorrhage [23].…”

Section: Introductionmentioning

confidence: 94%

Isoflurane but not Fentanyl Causes Apoptosis in Immature Primary Neuronal Cells

Berns¹,

Wolter²,

Bührer³

et al. 2017

TOATJ

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Background:Anaesthetics are widely used in new-borns and preterm infants, although it is known that they may adversely affect the developing brain. Objective:We assessed the impact of the volatile anaesthetic, isoflurane, and the intravenous analgesic, fentanyl, on immature and mature embryonic neuronal cells. Methods:Primary neuronal cultures from embryonic rats (E18) cultured for 5 (immature) or 15 days (mature) in vitro (DIV), respectively, were exposed to isoflurane (1.5 Vol.%) or fentanyl (0.8 -200 ng/ml) for 24 hours. Experiments were repeated in the presence of the γ-amino butyric acid-A (GABA A ) receptor antagonists, bicuculline or picrotoxin (0.1 mmol/l), or the pancaspase inhibitor zVAD-fmk (20 nmol/l). Cell viability was assessed by methyltetrazolium (MTT) metabolism or lactate dehydrogenase (LDH) release. Results:Isoflurane reduced cell viability significantly in primary neuronal cells cultured for 5 DIV (Δ MTT -28 ±13%, Δ LDH +143 ±15%). Incubation with bicuculline, picrotoxin or zVAD-fmk protected the cells mostly from isoflurane toxicity. After 15 DIV, cell viability was not reduced by isoflurane. Viability of primary neurons cultured for 5 DIV did not change with fentanyl over the wide range of concentrations tested. Conclusion:Immature primary neurons may undergo apoptosis following exposure to isoflurane but are unaffected by fentanyl. Mature primary neurons were not affected by isoflurane exposure.

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Section: Introductionmentioning

confidence: 94%

Isoflurane but not Fentanyl Causes Apoptosis in Immature Primary Neuronal Cells

Berns¹,

Wolter²,

Bührer³

et al. 2017

TOATJ

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“…The percentage of NeuN-positive neurons and GFAP-positive astrocytes was determined by counting the number of NeuN-and GFAP-positive cells in eight separate fields over two wells. Purity of neuronal cultures was 86 % neurons and 11 % astrocytes [18,19].…”

Section: Cell Culturementioning

confidence: 99%

“…LDH absorbance (492 nm) values from control were subtracted from sevoflurane post-conditioning of different concentrations and cell injury values were expressed as a percentage of total LDH (determined for each experiment by assaying the supernatant of duplicated cultures after 30 min of exposure to 1 % Triton X-100) caused by different concentrations of sevoflurane [17,18].…”

Section: Assessment Of Neuronal Injurymentioning

confidence: 99%

“…Real-time PCR was performed as described in our previous study [18]. Briefly, total RNA was extracted from neuronal cultures and 500 ng of RNA in each group was reversely transcribed into cDNA using oligo dT and superscript III reverse transcriptase (Invitrogen Corporation, Carlsbad, CA, USA) following the manufacturer's instructions.…”

Section: Real-time Pcr Assessment Of Bid Bim and Puma Mrna Expressionmentioning

confidence: 99%

“…After washing with PBS, nuclei were counterstained with Hoechst33342 (10 lg/mL) (Invitrogen, Grand Island, NY, USA). The number of PI-positive cells was counted in at least three separate experiments per treatment condition without the knowledge of treatment history [18].…”

Section: Assessment Of Neuronal Deathmentioning

confidence: 99%

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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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Increased Expression of Slit2 and its Robo Receptors During Astroglial Scar Formation After Transient Focal Cerebral Ischemia in Rats

et al. 2016

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Slit2, a secreted glycoprotein, has recently been implicated in the post-ischemic astroglial reaction. The objective of this study was to investigate the temporal changes and cellular localization of Slit2 and its receptors, Robo1, Robo2, and Robo4, in a rat transient focal ischemia model induced by middle cerebral artery occlusion. We used double- and triple-immunolabeling to determine the cell-specific changes in Slit2 and its receptors during a 10-week post-ischemia period. The expression profiles of Slit2 and the Robo receptors shared overlapping expression patterns in sham-operated and ischemic striatum. Constitutive expression of Slit2 and Robo receptors was observed in striatal neurons with weak intensity, whereas in rats reperfused after ischemic insults, these immunoreactivities were increased in reactive astrocytes. Astroglial induction of Slit2 and Robo in the peri-infarct region was distinct on days 7-14 after reperfusion and thereafter increased progressively throughout the 10-week experimental period. Slit2 and Robo were prominently expressed in the perinuclear cytoplasm and main processes of reactive astrocytes forming the astroglial scar. This observation was confirmed by quantification of the mean fluorescence intensity of Slit2 and Robo receptors over reactive astrocytes localized at the edge of the infarct area. However, activated microglia/macrophages in the peri-infarct area were devoid of any specific labeling for Slit2 and Robo. Thus, our data revealed a selective and sustained induction of Slit2 and Robo in astrocytes localized throughout the astroglial scar after ischemic stroke, suggesting that Slit2/Robo signaling participates in glial scar formation and brain remodeling following ischemic injury.

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Isoflurane post-conditioning protects primary cultures of cortical neurons against oxygen and glucose deprivation injury via upregulation of Slit2/Robo1

Cited by 15 publications

References 34 publications

Isoflurane but not Fentanyl Causes Apoptosis in Immature Primary Neuronal Cells

Isoflurane but not Fentanyl Causes Apoptosis in Immature Primary Neuronal Cells

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

Increased Expression of Slit2 and its Robo Receptors During Astroglial Scar Formation After Transient Focal Cerebral Ischemia in Rats

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