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Role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygenglucose deprivation injury in rat hippocampal slices

Yonghua Zhang, Qiuping Chen, Xuelian Huang, Su Cao

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Abstract

Objective To evaluate the role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygen-glucose deprivation(OGD)injury in rat hippocampal slices.Methods Male adult SD rats weighing 80-100 g were anesthetized with ether and decapitated.The hippocampi were removed and sagittally sliced(400μm thick)and placed in artificial cerebrospinal fluid(aCSF)aerated with 95% O2-5%CO2.Fifty hippoeampal slices were randomly divided into 5 groups(t =10 each):OGD group; 4% sevoflurane postconditioning group(group Sevo); PD98059(specific inhibitor of ERK)group(group PD); dimethyl sulfoxide (DMSO)group; 4% sevoflurane postconditioning + PD98059 group(group SPD).OGD was induced by incubating the slices in glucose-free aCSF aerated with 95% N2-5% CO2 for 15 min in group OGD.The hippocampal slices were perfused with aCSF saturated with 4% sevoflurane for 30 min after OGD was induced in group Sevo.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L for 10 min after OGD was induced in group PD.The hippocampal slices were perfused with aCSF containing DMSO 1 mol/L for 10 min after OGD was induced in group DMSO.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L and aerated with 4% sevoflurane for 30 min after OGD was induced in group SPD.The hippocampal slices were then perfused with plain aCSF for 1 h again in all the groups.The electrophysiological technique was used 1o record the amplitude of orthodromic population spike(OPS)in the stralum pyramidale of the CAI region.TTC staining was used to determine the degree of tissue injury.Results Compared with group OGD,the recovery amplitude and rate of OPS were significantly increased,and the degree of tissue injury was significantly decreased in group Sevo(P <0.01),while no significant change was found in each parameter in the other three groups(P > 0.05).Compared with group Sevo,the recovery amplitude and tale of OPS were significandy decreased,and the degree of tissue injury was significantly increased in groups PD,DMSO and SPD(P < 0.01).Conclusion ERK1/2 signal transduction pathway is involved in sevoflurane postcondilioning-induced reduction of OGD injury in tat hippocampal slices. Key words: Extracellular signal-regulated MAP kinases; Anesthetics, inhalation; Hippocampus; Anoxia

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Objective To evaluate the role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygen-glucose deprivation(OGD)injury in rat hippocampal slices.Methods Male adult SD rats weighing 80-100 g were anesthetized with ether and decapitated.The hippocampi were removed and sagittally sliced(400μm thick)and placed in artificial cerebrospinal fluid(aCSF)aerated with 95% O2-5%CO2.Fifty hippoeampal slices were randomly divided into 5 groups(t =10 each):OGD group; 4% sevoflurane postconditioning group(group Sevo); PD98059(specific inhibitor of ERK)group(group PD); dimethyl sulfoxide (DMSO)group; 4% sevoflurane postconditioning + PD98059 group(group SPD).OGD was induced by incubating the slices in glucose-free aCSF aerated with 95% N2-5% CO2 for 15 min in group OGD.The hippocampal slices were perfused with aCSF saturated with 4% sevoflurane for 30 min after OGD was induced in group Sevo.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L for 10 min after OGD was induced in group PD.The hippocampal slices were perfused with aCSF containing DMSO 1 mol/L for 10 min after OGD was induced in group DMSO.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L and aerated with 4% sevoflurane for 30 min after OGD was induced in group SPD.The hippocampal slices were then perfused with plain aCSF for 1 h again in all the groups.The electrophysiological technique was used 1o record the amplitude of orthodromic population spike(OPS)in the stralum pyramidale of the CAI region.TTC staining was used to determine the degree of tissue injury.Results Compared with group OGD,the recovery amplitude and rate of OPS were significantly increased,and the degree of tissue injury was significantly decreased in group Sevo(P <0.01),while no significant change was found in each parameter in the other three groups(P > 0.05).Compared with group Sevo,the recovery amplitude and tale of OPS were significandy decreased,and the degree of tissue injury was significantly increased in groups PD,DMSO and SPD(P < 0.01).Conclusion ERK1/2 signal transduction pathway is involved in sevoflurane postcondilioning-induced reduction of OGD injury in tat hippocampal slices. Key words: Extracellular signal-regulated MAP kinases; Anesthetics, inhalation; Hippocampus; Anoxia

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Available abstract

Objective To evaluate the role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygen-glucose deprivation(OGD)injury in rat hippocampal slices.Methods Male adult SD rats weighing 80-100 g were anesthetized with ether and decapitated.The hippocampi were removed and sagittally sliced(400μm thick)and placed in artificial cerebrospinal fluid(aCSF)aerated with 95% O2-5%CO2.Fifty hippoeampal slices were randomly divided into 5 groups(t =10 each):OGD group; 4% sevoflurane postconditioning group(group Sevo); PD98059(specific inhibitor of ERK)group(group PD); dimethyl sulfoxide (DMSO)group; 4% sevoflurane postconditioning + PD98059 group(group SPD).OGD was induced by incubating the slices in glucose-free aCSF aerated with 95% N2-5% CO2 for 15 min in group OGD.The hippocampal slices were perfused with aCSF saturated with 4% sevoflurane for 30 min after OGD was induced in group Sevo.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L for 10 min after OGD was induced in group PD.The hippocampal slices were perfused with aCSF containing DMSO 1 mol/L for 10 min after OGD was induced in group DMSO.The hippocampal slices were perfused with aCSF containing PD98059 50 μmol/L and aerated with 4% sevoflurane for 30 min after OGD was induced in group SPD.The hippocampal slices were then perfused with plain aCSF for 1 h again in all the groups.The electrophysiological technique was used 1o record the amplitude of orthodromic population spike(OPS)in the stralum pyramidale of the CAI region.TTC staining was used to determine the degree of tissue injury.Results Compared with group OGD,the recovery amplitude and rate of OPS were significantly increased,and the degree of tissue injury was significantly decreased in group Sevo(P <0.01),while no significant change was found in each parameter in the other three groups(P > 0.05).Compared with group Sevo,the recovery amplitude and tale of OPS were significandy decreased,and the degree of tissue injury was significantly increased in groups PD,DMSO and SPD(P < 0.01).Conclusion ERK1/2 signal transduction pathway is involved in sevoflurane postcondilioning-induced reduction of OGD injury in tat hippocampal slices. Key words: Extracellular signal-regulated MAP kinases; Anesthetics, inhalation; Hippocampus; Anoxia

Key concepts: Hippocampal formation, Sevoflurane, Population spike, Anesthesia, Chemistry, Dimethyl sulfoxide, Pharmacology, Endocrinology

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Role of ERK1/2 signal transduction pathway in sevoflurane postconditioning-induced reduction of oxygenglucose deprivation injury in rat hippocampal slices — Research Paper | ScholarLens