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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.
J Neurol Sci 2015; 357(1-2):80-7JN

Abstract

Temporal post-conditioning helps provide neuroprotection against brain injury secondary to ischemia-reperfusion and is considered an effective intervention, but the exact mechanism of sevoflurane post-conditioning is unclear. The essential axis involves activator Bid, Bim, Puma (BH3s), Bax, and Bak; activates the mitochondrial death program; and might be involved in a cell death signal. Extracellular signal-related kinases 1/2 (Erk1/2) play a pivotal role in cell growth and proliferation. We hypothesized that sevoflurane post-conditioning might inhibit Bid, Bim, Puma, Bax, and Bak expression and is activated by phosphor-Erk1/2 to decrease neuronal death. To test this hypothesis, we exposed primary cortical neuron cultures to oxygen-glucose deprivation for 1h, along with resuscitation for 24h (OGD/R). MTT assays, propidium iodide uptake (PI), JC-1 fluorescence, and Western blot indicated the following: decreased cell viability (P<0.05); increased cell death (P<0.05); decreased mitochondrial membrane potential (P<0.05); and decreased Bid, Bim, Puma, Bax, and Bak expression with OGD/R exposure. Inhibition of Erk1/2 phosphorylation could attenuate sevoflurane post-conditioning that mediated an increase in neuronal viability and mitochondrial membrane potential, as well as a decrease in cell death and Bid, Bim, Puma, Bax, and Bak expression after OGD/R treatment. The results demonstrated that sevoflurane post-conditioning caused a marked decrease in cortical neuronal death secondary to OGD/R exposure through the downregulation of the mitochondrial apoptosis axis involving Bid, Bim, Puma, Bax, and Bak that was mediated by the phosphorylation/activation of Erk1/2.

Authors+Show Affiliations

Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China. Electronic address: azai2015@126.com.Department of Anesthesiology, Shengjing Hospital, China Medical University, Shenyang, China.Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China.Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China.Department of Anesthesiology, First Affiliated Hospital, China Medical University, Shenyang, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26152828

Citation

Zhang, Li-Min, et al. "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." Journal of the Neurological Sciences, vol. 357, no. 1-2, 2015, pp. 80-7.
Zhang LM, Zhao XC, Sun WB, et al. 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. J Neurol Sci. 2015;357(1-2):80-7.
Zhang, L. M., Zhao, X. C., Sun, W. B., Li, R., & Jiang, X. J. (2015). 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. Journal of the Neurological Sciences, 357(1-2), pp. 80-7. doi:10.1016/j.jns.2015.06.070.
Zhang LM, et al. 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. J Neurol Sci. 2015 Oct 15;357(1-2):80-7. PubMed PMID: 26152828.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Zhang,Li-Min, AU - Zhao,Xiao-Chun, AU - Sun,Wen-Bo, AU - Li,Rui, AU - Jiang,Xiao-Jing, Y1 - 2015/07/02/ PY - 2015/02/02/received PY - 2015/06/29/revised PY - 2015/06/30/accepted PY - 2015/7/9/entrez PY - 2015/7/15/pubmed PY - 2016/9/14/medline KW - Bak KW - Bax KW - Bid KW - Bim KW - Extracellular signal-related kinases 1/2 KW - Neuroprotection KW - Puma KW - Sevoflurane SP - 80 EP - 7 JF - Journal of the neurological sciences JO - J. Neurol. Sci. VL - 357 IS - 1-2 N2 - Temporal post-conditioning helps provide neuroprotection against brain injury secondary to ischemia-reperfusion and is considered an effective intervention, but the exact mechanism of sevoflurane post-conditioning is unclear. The essential axis involves activator Bid, Bim, Puma (BH3s), Bax, and Bak; activates the mitochondrial death program; and might be involved in a cell death signal. Extracellular signal-related kinases 1/2 (Erk1/2) play a pivotal role in cell growth and proliferation. We hypothesized that sevoflurane post-conditioning might inhibit Bid, Bim, Puma, Bax, and Bak expression and is activated by phosphor-Erk1/2 to decrease neuronal death. To test this hypothesis, we exposed primary cortical neuron cultures to oxygen-glucose deprivation for 1h, along with resuscitation for 24h (OGD/R). MTT assays, propidium iodide uptake (PI), JC-1 fluorescence, and Western blot indicated the following: decreased cell viability (P<0.05); increased cell death (P<0.05); decreased mitochondrial membrane potential (P<0.05); and decreased Bid, Bim, Puma, Bax, and Bak expression with OGD/R exposure. Inhibition of Erk1/2 phosphorylation could attenuate sevoflurane post-conditioning that mediated an increase in neuronal viability and mitochondrial membrane potential, as well as a decrease in cell death and Bid, Bim, Puma, Bax, and Bak expression after OGD/R treatment. The results demonstrated that sevoflurane post-conditioning caused a marked decrease in cortical neuronal death secondary to OGD/R exposure through the downregulation of the mitochondrial apoptosis axis involving Bid, Bim, Puma, Bax, and Bak that was mediated by the phosphorylation/activation of Erk1/2. SN - 1878-5883 UR - https://www.unboundmedicine.com/medline/citation/26152828/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-510X(15)00421-9 DB - PRIME DP - Unbound Medicine ER -