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Erythropoietin rescues primary rat cortical neurons from pyroptosis and apoptosis via Erk1/2-Nrf2/Bach1 signal pathway.
Brain Res Bull. 2017 04; 130:236-244.BR

Abstract

The most commonly used inhalation anesthetics, sevoflurane, is reported to be a risk for development of learning disability. Erythropoietin (EPO) administration might be involved an effective therapy for sevoflurane neurotoxicity. EPO-EPO receptor-extracellular signal-related kinases 1/2 (Erk1/2) signal pathway plays a pivotal role in the neuroprotective effect. Nuclear factor erythroid 2-related factor (Nrf2)/BTB and CNC homology 1 (Bach1) ratio altering by Erk1/2 could ameliorate oxidative stress occurred in human macrophages. Primary cortical neuron cultures exposed to sevoflurane were assessed for cleaved caspase-1, cleaved caspase-3, Nrf2, Bach1, total Erk1/2, and phosphorylated Erk1/2 with the following: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT); propidium iodide uptake (PI); lactate dehydrogenase (LDH); malondialdehyde (MDA); superoxide dismutase (SOD); Real-time PCR; and Western blot. We found that sevoflurane exposure increased cell pyroptosis, apoptosis, injury, and MDA (n=9, P<0.05), but decreased cell viability (n=9, P<0.05) and down-regulated SOD (n=9, P<0.05), while EPO partially rescued the neurotoxicity induced by sevoflurane (n=9, P<0.05), as well as increase the expression of Nrf2 mRNA and Nrf2/Bach1 ratio (n=9, P<0.05). Inhibition of Erk1/2 phosphorylation via PD98059 reversed the protective effect of EPO (n=9, P<0.05). Thus, protection of EPO markedly attenuated pyroptosis and apoptosis of neurons exposed to sevoflurane via Erk1/2-Nrf2/Bach1 signal pathway.

Authors+Show Affiliations

Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China. Electronic address: azai2005@sina.com.Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China. Electronic address: azai2010@126.com.Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China. Electronic address: 406403979@qq.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28189515

Citation

Li, Rui, et al. "Erythropoietin Rescues Primary Rat Cortical Neurons From Pyroptosis and Apoptosis Via Erk1/2-Nrf2/Bach1 Signal Pathway." Brain Research Bulletin, vol. 130, 2017, pp. 236-244.
Li R, Zhang LM, Sun WB. Erythropoietin rescues primary rat cortical neurons from pyroptosis and apoptosis via Erk1/2-Nrf2/Bach1 signal pathway. Brain Res Bull. 2017;130:236-244.
Li, R., Zhang, L. M., & Sun, W. B. (2017). Erythropoietin rescues primary rat cortical neurons from pyroptosis and apoptosis via Erk1/2-Nrf2/Bach1 signal pathway. Brain Research Bulletin, 130, 236-244. https://doi.org/10.1016/j.brainresbull.2017.01.016
Li R, Zhang LM, Sun WB. Erythropoietin Rescues Primary Rat Cortical Neurons From Pyroptosis and Apoptosis Via Erk1/2-Nrf2/Bach1 Signal Pathway. Brain Res Bull. 2017;130:236-244. PubMed PMID: 28189515.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Erythropoietin rescues primary rat cortical neurons from pyroptosis and apoptosis via Erk1/2-Nrf2/Bach1 signal pathway. AU - Li,Rui, AU - Zhang,Li-Min, AU - Sun,Wen-Bo, Y1 - 2017/02/09/ PY - 2016/09/25/received PY - 2017/01/11/revised PY - 2017/01/24/accepted PY - 2017/2/13/pubmed PY - 2018/2/23/medline PY - 2017/2/13/entrez KW - Apoptosis KW - Erythropoietin KW - Neurotoxicity KW - Pyroptosis KW - Sevoflurane SP - 236 EP - 244 JF - Brain research bulletin JO - Brain Res. Bull. VL - 130 N2 - The most commonly used inhalation anesthetics, sevoflurane, is reported to be a risk for development of learning disability. Erythropoietin (EPO) administration might be involved an effective therapy for sevoflurane neurotoxicity. EPO-EPO receptor-extracellular signal-related kinases 1/2 (Erk1/2) signal pathway plays a pivotal role in the neuroprotective effect. Nuclear factor erythroid 2-related factor (Nrf2)/BTB and CNC homology 1 (Bach1) ratio altering by Erk1/2 could ameliorate oxidative stress occurred in human macrophages. Primary cortical neuron cultures exposed to sevoflurane were assessed for cleaved caspase-1, cleaved caspase-3, Nrf2, Bach1, total Erk1/2, and phosphorylated Erk1/2 with the following: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT); propidium iodide uptake (PI); lactate dehydrogenase (LDH); malondialdehyde (MDA); superoxide dismutase (SOD); Real-time PCR; and Western blot. We found that sevoflurane exposure increased cell pyroptosis, apoptosis, injury, and MDA (n=9, P<0.05), but decreased cell viability (n=9, P<0.05) and down-regulated SOD (n=9, P<0.05), while EPO partially rescued the neurotoxicity induced by sevoflurane (n=9, P<0.05), as well as increase the expression of Nrf2 mRNA and Nrf2/Bach1 ratio (n=9, P<0.05). Inhibition of Erk1/2 phosphorylation via PD98059 reversed the protective effect of EPO (n=9, P<0.05). Thus, protection of EPO markedly attenuated pyroptosis and apoptosis of neurons exposed to sevoflurane via Erk1/2-Nrf2/Bach1 signal pathway. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/28189515/Erythropoietin_rescues_primary_rat_cortical_neurons_from_pyroptosis_and_apoptosis_via_Erk1/2_Nrf2/Bach1_signal_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(16)30289-1 DB - PRIME DP - Unbound Medicine ER -