Sevoflurane and Isoflurane Preconditioning Provides Neuroprotection by Inhibition of Apoptosis-related mRNA Expression in a Rat Model of Focal Cerebral Ischemia

Bedirli, Nurdan; Bagriacik, Emin Umit; Emmez, Hakan; Yılmaz, Güldal; Ünal, Yusuf; Özköse, Zerrin

doi:10.1097/ana.0b013e318266791e

Cited by 71 publications

(47 citation statements)

References 37 publications

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“…Similarly, isoflurane inhibits the aforementioned proinflammatory cytokine production in lung tissue and suppresses apoptosis by downregulating procaspases 3 and 8 and caspases 3 and 8 (Li et al 2013b). Notably, both SEV and isoflurane ameliorate inflammation, but SEV is significantly more inhibitory than isoflurane in this respect (Bedirli et al 2012). …”

Section: Discussionmentioning

confidence: 99%

Plasma Kynurenic Acid Concentration in Patients Undergoing Cardiac Surgery: Effect of Anaesthesia

Kotlińska-Hasiec

Nowicka-Stążka

Parada-Turska

et al. 2014

Arch. Immunol. Ther. Exp.

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Increases in plasma kynurenic acid (KYNA) concentration relate to the severity of inflammation. The aim of this study was to analyse changes in plasma KYNA concentration and neutrophil/lymphocyte ratio (NLR) in cardiac surgery patients. Additionally, the effect of anaesthesia was analysed. Adult cardiac surgery patients under intravenous general anaesthesia were studied. Additionally, some patients received sevoflurane (SEV) prior to cardiopulmonary bypass. Plasma KYNA concentration and NLR were measured before anaesthesia, just after surgery and on postoperative days 1, 2 and 3. Patients were assigned to two groups: patients who did not receive SEV (NonSEV group) and patients who received SEV (SEV group). Forty-three patients were studied. Twenty-four of them received SEV. KYNA increased immediately after surgery and remained elevated through postoperative day 3 in the NonSEV group, whereas it was similar to the preoperative concentration in the SEV group. NLR increased immediately after surgery in both groups, and higher values were noted in the NonSEV group than in the SEV group at postoperative days 2 and 3. Plasma KYNA concentration correlated with NLR in the NonSEV group. Cardiac surgery caused an increase in NLR. Plasma KYNA increased in the NonSEV group and correlated with NLR. Administration of SEV inhibited the increase in KYNA, most likely due to its anti-inflammatory properties.

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Section: Discussionmentioning

confidence: 99%

Plasma Kynurenic Acid Concentration in Patients Undergoing Cardiac Surgery: Effect of Anaesthesia

Kotlińska-Hasiec

Nowicka-Stążka

Parada-Turska

et al. 2014

Arch. Immunol. Ther. Exp.

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“…However, the mechanisms of the neuroprotective effects of sevoflurane have been poorly elucidated. Some results show that sevoflurane partially inhibits apoptosis through downregulation of proapoptotic genes (such as Tnf and Tp53) and upregulation of antiapoptotic genes (such as Bcl-2 and Prok2) [9]. Others believe that sevoflurane preconditioning induces neuroprotection by releasing ROS and inducing the consequent upregulation of antioxidant enzymes such as GSH-px [10].…”

Section: Introductionmentioning

confidence: 96%

Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

Wen

Liu

et al. 2015

Mol Neurobiol

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In this study, we investigated the neuroprotective effect of sevoflurane against ischemic brain injury and its underlying molecular mechanisms. Transient global brain ischemia was induced by 4-vessel occlusion in adult male Sprague-Dawley rats. The rats were pretreated with sevoflurane alone or sevoflurane combined with LY294002/wortmannin (selective inhibitor of PI3K) before ischemia. Cresyl violet staining was used to examine the survival of hippocampal CA1 pyramidal neurons. Immunoblotting and immunoprecipitation were performed to measure the phosphorylation of Akt1, PRAS40, ASK1, and JNK3 and the expression of cleaved-caspase-3. The results demonstrated that a moderate dose of sevoflurane inhalation of 2% for 2 h had significant neuroprotective effects against ischemia/reperfusion induced hippocampal neuron death. Sevoflurane significantly increased Akt and PRAS40 phosphorylation and decreased the phosphorylation of ASK1 at 6 h after reperfusion and the phosphorylation of JNK3 at 3 days after reperfusion following 15 min of transient global brain ischemia. Conversely, LY294002 and wortmannin significantly inhibited the effects of sevoflurane. Taken together, the results suggest that sevoflurane could suppress ischemic brain injury by downregulating the activation of the ASK1/JNK3 cascade via increasing the phosphorylation of Akt1 during ischemia/reperfusion.

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“…ISO was purchased from Abbott Laboratories (North Chicago, IL, USA) and was stored in the dark. Pretreatment with 2% ISO for 60 min was deemed sufficient to induce ischemic tolerance (16,17). Male Sprague-Dawley rats weighing between 250 and 270 g were provided by the Experimental Animal Center of the Fourth Military Medical University (Xi'an, China).…”

Section: Methodsmentioning

confidence: 99%

Protective role of isoflurane pretreatment in rats with focal cerebral ischemia and the underlying molecular mechanism

Xiao

Ren

Yang

et al. 2012

Molecular Medicine Reports

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Abstract. Inflammation and immunity are important in the pathogenesis of cerebral ischemia. Toll-like receptor 4 (TLR4) is involved in the inflammatory responses of injured brain tissues. Emerging studies have focused on the effect of isoflurane (ISO) pretreatment on cerebral ischemia, however, the association between ISO pretreatment and TLR4 during cerebral ischemia remains to be elucidated. In the present study, the protective role of ISO pretreatment in rats with focal cerebral ischemia reperfusion was investigated and the molecular mechanism was discussed. Using a middle cerebral artery occlusion (MCAO) model, triphenyltetrazolium chloride staining was utilized to measure the infarct volume and brain edema and immunofluorescence staining was used to detect the MCAO-induced TLR4 expression and localization. Western blot analyses were conducted to quantify the protein expression levels of TLR4, myeloid differentiation primary response 88 (MyD88) and nuclear factor (NF)-κB in ischemic brain tissue at different time points. The results demonstrated that, following ISO pretreatment, the neurological deficits, brain edema and cerebral infarct size caused by ischemia/reperfusion were attenuated. The astrocyte and microglial activation in the brain tissue was decreased. In addition, the expression levels of TLR4, MyD88 and NF-κB were decreased. The present study indicated that ISO pretreatment may protect the brain from ischemic damage by downregulating the expression levels of TLR4, MyD88 and NF-κB.

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Sevoflurane and Isoflurane Preconditioning Provides Neuroprotection by Inhibition of Apoptosis-related mRNA Expression in a Rat Model of Focal Cerebral Ischemia

Abstract: Sevoflurane and isoflurane preconditioning ameliorates inflammation, cerebral lipid peroxidation, and histologic injury. Downregulation of proapoptotic molecules and upregulation of antiapoptotic molecules may be associated with this effect.

Cited by 71 publications

References 37 publications

Plasma Kynurenic Acid Concentration in Patients Undergoing Cardiac Surgery: Effect of Anaesthesia

Plasma Kynurenic Acid Concentration in Patients Undergoing Cardiac Surgery: Effect of Anaesthesia

Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

Protective role of isoflurane pretreatment in rats with focal cerebral ischemia and the underlying molecular mechanism

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