Sevoflurane Protects Rat Mixed Cerebrocortical Neuronal–Glial Cell Cultures against Transient Oxygen–Glucose Deprivation

Canas, Paula T.; Velly, Lionel; Labrande, Christelle N.; Guillet, Benjamin; Sautou, V.; Masmejean, F.; Nieoullon, A.; Gouin, F; Bruder, Nicolas; Pisano, Pascale

doi:10.1097/00000542-200611000-00021

Cited by 37 publications

(20 citation statements)

References 39 publications

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“…[19] Sevoflurane, in contrast to isoflurane, mediates neuronal preconditioning not only with mitochondrial K ATP channels, [11] but also with enhanced phosphorylated cyclic adenosine monophosphate response element binding protein signaling, [20] by downregulating tumor necrosis factor-α, interleukin-1 β protein and messenger RNA expression, [21] and decrease in reactive oxygen species generation during re-oxygenation. [22] DO2I was significantly higher in patients receiving volatile anesthetic agents than those undergoing TIVA. This might be secondary to decreased SVRI, compared to the TIVA group, observed in volatile anesthetic agent groups thereby leading to enhanced perfusion and better tissue oxygen delivery.…”

Section: Discussionmentioning

confidence: 83%

Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques

et al. 2011

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Cardiac surgery with aid of cardiopulmonary bypass (CPB) is associated with neurological dysfunction. The presence of cerebrospecific protein S100β in serum is an indicator of cerebral damage. This study was designed to evaluate the influence of three different anesthesia techniques, on S100β levels, in patients undergoing coronary artery bypass grafting on CPB. A total of 180 patients were divided into three groups - each of who received sevoflurane, isoflurane and total intravenous anesthesia as part of the anesthetic technique, respectively. S100 were evaluated from venous sample at following time intervals - prior to induction of anesthesia (T1), after coming off CPB (T2); 12 h after aortic cross clamping (T3) and 24 h after aortic cross clamping (T4). In all three groups, maximal rise in S100β levels occurred after CPB which gradually declined over next 24 h, the levels at 24 h post-AOXC being significantly higher than baseline levels. Significantly low levels of S100β were noted at all postdose hours in the sevoflurane group, as compared to the total intravenous anesthesia (TIVA) group, and at 12 and 24 h postaortic cross clamp, in comparison to the isoflurane group. Comparing the isoflurane group with the TIVA group, the S100 levels were lower in the isoflurane group only at 24 h postaortic cross clamp. It was concluded that maximum rise in S100β levels occurs immediately after CPB with a gradual decline in next 24 h. The rise in S100β levels is significantly less in patients administered sevoflurane in comparison to isoflurane or TIVA. Hemodynamic parameters had no influence on the S100β levels during the first 24 h after surgery.

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Section: Discussionmentioning

confidence: 83%

Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques

et al. 2011

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“…Primary hippocampal neuron cultures, microglial cell cultures, mixed neuronalglial cell cultures, and OGD were performed as previously described (14,26). In brief, the cell cultures were prepared from neonatal mice, and the hippocampi and cortices were dissected and dissociated with 0.25% trypsin-EDTA (Life Technologies, Birmingham, MI).…”

Section: Cell Cultures and Ogdmentioning

confidence: 99%

Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Wang

Huang

Chen

et al. 2014

The Journal of Immunology

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Recent reports have shown that preconditioning with the TLR3 ligand polyinosinic-polycytidylic acid (poly(I:C)) protects against cerebral ischemia/reperfusion (I/R) injury. However, it is unclear whether poly(I:C) treatment after cerebral I/R injury is also effective. We used mouse/rat middle cerebral artery occlusion and cell oxygen-glucose deprivation models to evaluate the therapeutic effects and mechanisms of poly(I:C) treatment. Poly(I:C) was i.p. injected 3 h after ischemia (treatment group). Cerebral infarct volumes and brain edemas were significantly reduced, and neurologic scores were significantly increased. TNF-α and IL-1β levels were markedly decreased, whereas IFN-β levels were greatly increased, in the ischemic brain tissues, cerebral spinal fluid, and serum. Injuries to hippocampal neurons and mitochondria were greatly reduced. The numbers of TUNEL-positive and Fluoro-Jade B+ cells also decreased significantly in the ischemic brain tissues. Poly(I:C) treatment increased the levels of Hsp27, Hsp70, and Bcl2 and decreased the level of Bax in the ischemic brain tissues. Moreover, poly(I:C) treatment attenuated the levels of TNF-α and IL-1β in serum and cerebral spinal fluid of mice stimulated by LPS. However, the protective effects of poly(I:C) against cerebral ischemia were abolished in TLR3−/− and TLR4−/−mice. Poly(I:C) downregulated TLR4 signaling via TLR3. Poly(I:C) treatment exhibited obvious protective effects 14 d after ischemia and was also effective in the rat permanent middle cerebral artery occlusion model. The results suggest that poly(I:C) exerts therapeutic effects against cerebral I/R injury through the downregulation of TLR4 signaling via TLR3. Poly(I:C) is a promising new drug candidate for the treatment of cerebral infarcts.

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“…Cells were maintained in the anaerobic chamber at 37 • C for 2 h to produce oxygen deprivation. The duration of OGD was chosen according to previous studies (Zhang et al, 2003;Canas et al, 2006). Control cells not exposed to OGD were maintained in DMEM containing glucose (20 mM) and aerated with aerobic gas mixture (95% air, 5% CO 2 ).…”

Section: Oxygen and Glucose Deprivation (Ogd) Followed By Reoxygenationmentioning

confidence: 99%

“…Neuronal injury or death was assessed by morphological examination using phase-contrast microscopy and quantified by measuring the amount of LDH released into the extracellular medium as previously described (Bosel et al, 2005;Canas et al, 2006). Briefly, reaction mixture (100 l) was added to conditioned media (100 l) removed from 24-well plates after centrifugation at 250 × g for 10 min.…”

Section: Lactate Dehydrogenase (Ldh) Release Assaymentioning

confidence: 99%

Neuroprotective effects of water-soluble Ganoderma lucidum polysaccharides on cerebral ischemic injury in rats

Zhou

Tang

Xiang

et al. 2010

Journal of Ethnopharmacology

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Sevoflurane Protects Rat Mixed Cerebrocortical Neuronal–Glial Cell Cultures against Transient Oxygen–Glucose Deprivation

Cited by 37 publications

References 39 publications

Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques

Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques

Polyinosinic-Polycytidylic Acid Has Therapeutic Effects against Cerebral Ischemia/Reperfusion Injury through the Downregulation of TLR4 Signaling via TLR3

Neuroprotective effects of water-soluble Ganoderma lucidum polysaccharides on cerebral ischemic injury in rats

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