We are analyzing https://link.springer.com/article/10.1007/s12640-016-9631-7.

Title:
β-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38MAPK–p53 Signaling Pathway | Neurotoxicity Research
Description:
Parkinson’s disease (PD) is a neurological disorder pathologically characterized by loss of dopaminergic neurons in the substantia nigra. No curative therapy is available for PD. We recently found that phytoestrogen β-ecdysterone (β-Ecd) is able to reduce MPP+-induced apoptosis in PC12 cells. This study investigated the potential of β-Ecd to protect against SH-SY5Y cell apoptosis induced by the PD-related neurotoxin 6-hydroxydopamine (6-OHDA) and the underlying mechanism for this cytoprotection. In the present study, pretreatment with β-Ecd significantly reduced 6-OHDA-induced apoptosis of SH-SY5Y cells by a mitochondria-dependent pathway, as indicated by downregulation of Bax and PUMA (p53 upregulated modulator of apoptosis) expression, suppressing ΔΨm loss, inhibiting cytochrome c release, and attenuating caspase-9 activation. Furthermore, we showed that the inhibition of p38 mitogen-activated protein kinase (p38MAPK)-dependent p53 promoter activity contributed to the protection of SH-SY5Y cells from apoptosis, which was validated by the use of SB203580 or p38β dominant negative (DN) mutants. Additionally, knock-down apoptosis signal-regulating kinase 1 (ASK1) by specific shRNA and blockade reactive oxygen species (ROS) by pharmacological inhibitor competently prevented β-Ecd-mediated inhibition of p38MAPK and ASK1 phosphorylation, respectively. These data provide the first evidence that β-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1–p38MAPK pathways. The neuroprotective effects of β-Ecd make it a promising candidate as a therapeutic agent for PD.
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Keywords {🔍}

pubmed, article, google, scholar, cas, parkinsons, disease, apoptosis, cells, cell, shsyy, pathway, central, zhang, dong, dopaminergic, neurons, mitochondrial, research, inhibition, reactive, oxygen, access, wang, content, protects, kinase, species, kim, privacy, cookies, βecdysterone, hydroxydopamineinduced, signaling, miaoxian, loss, substantia, nigra, βecd, protein, death, biol, neuronal, data, protection, information, publish, search, neurotoxicity, mechanism,

Topics {✒️}

prolyl-isomerase pin1-mediated isomerization nf-κb signaling pathway month download article/chapter ros-dependent ask1–p38mapk pathways reduce mpp+-induced apoptosis neuroblastoma cells sh-sy5y neuroblastoma sh-sy5y cells p38mapk–p53 signaling pathway phytoestrogen β-ecdysterone mpp+-induced neurotoxicity p53-dependent apoptosis induced natural products research manganese-induced mitochondrial dysfunction protein l-isoaspartyl methyltransferase pi3k-nrf2-regulated pathway reactive oxygen species pd-related neurotoxin 6-hydroxydopamine xiaojie zhang & miaoxian dong sh-sy5y cells suppressing δψm loss high-content discovery strategies 6-ohda-induced apoptosis mitochondria-mediated pathway full article pdf β-ecd make substantia nigra cells mitochondria-dependent pathway rho kinase mediates protein l-isoaspartyl stress-induced environments oxidative stress triggered mitochondrial apoptosis pathway p38 mapk-mediated privacy choices/manage cookies 6-hydroxydopamine-induced apoptosis dopaminergic neurodegeneration linked related subjects fernandez-gomez fj substantia nigra leads intrinsic apoptosis pathway 6-hydroxydopamine-induced injury rotenone-induced cellular cdk5-mediated phosphorylation β-ecd disrupt p53 binding p53 transcription-dependent dopamine-induced apoptosis mitochondria-dependent mechanism article pan p53-independent manner

Questions {❓}

Alves da Costa C, Checler F (2011) Apoptosis in Parkinson’s disease: is p53 the missing link between genetic and sporadic Parkinsonism?
Cao J, Ying M, Xie N, Lin G, Dong R, Zhang J, Yan H, Yang X, He Q, Yang B (2014) The oxidation states of DJ-1 dictate the cell fate in response to oxidative stress triggered by 4-hpr: autophagy or apoptosis?
Hartmann A, Michel PP, Troadec JD, Mouatt-Prigent A, Faucheux BA, Ruberg M, Agid Y, Hirsch EC (2001) Is Bax a mitochondrial mediator in apoptotic death of dopaminergic neurons in Parkinson’s disease?

Schema {🗺️}

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         description:Parkinson’s disease (PD) is a neurological disorder pathologically characterized by loss of dopaminergic neurons in the substantia nigra. No curative therapy is available for PD. We recently found that phytoestrogen β-ecdysterone (β-Ecd) is able to reduce MPP+-induced apoptosis in PC12 cells. This study investigated the potential of β-Ecd to protect against SH-SY5Y cell apoptosis induced by the PD-related neurotoxin 6-hydroxydopamine (6-OHDA) and the underlying mechanism for this cytoprotection. In the present study, pretreatment with β-Ecd significantly reduced 6-OHDA-induced apoptosis of SH-SY5Y cells by a mitochondria-dependent pathway, as indicated by downregulation of Bax and PUMA (p53 upregulated modulator of apoptosis) expression, suppressing ΔΨm loss, inhibiting cytochrome c release, and attenuating caspase-9 activation. Furthermore, we showed that the inhibition of p38 mitogen-activated protein kinase (p38MAPK)-dependent p53 promoter activity contributed to the protection of SH-SY5Y cells from apoptosis, which was validated by the use of SB203580 or p38β dominant negative (DN) mutants. Additionally, knock-down apoptosis signal-regulating kinase 1 (ASK1) by specific shRNA and blockade reactive oxygen species (ROS) by pharmacological inhibitor competently prevented β-Ecd-mediated inhibition of p38MAPK and ASK1 phosphorylation, respectively. These data provide the first evidence that β-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1–p38MAPK pathways. The neuroprotective effects of β-Ecd make it a promising candidate as a therapeutic agent for PD.
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      description:Parkinson’s disease (PD) is a neurological disorder pathologically characterized by loss of dopaminergic neurons in the substantia nigra. No curative therapy is available for PD. We recently found that phytoestrogen β-ecdysterone (β-Ecd) is able to reduce MPP+-induced apoptosis in PC12 cells. This study investigated the potential of β-Ecd to protect against SH-SY5Y cell apoptosis induced by the PD-related neurotoxin 6-hydroxydopamine (6-OHDA) and the underlying mechanism for this cytoprotection. In the present study, pretreatment with β-Ecd significantly reduced 6-OHDA-induced apoptosis of SH-SY5Y cells by a mitochondria-dependent pathway, as indicated by downregulation of Bax and PUMA (p53 upregulated modulator of apoptosis) expression, suppressing ΔΨm loss, inhibiting cytochrome c release, and attenuating caspase-9 activation. Furthermore, we showed that the inhibition of p38 mitogen-activated protein kinase (p38MAPK)-dependent p53 promoter activity contributed to the protection of SH-SY5Y cells from apoptosis, which was validated by the use of SB203580 or p38β dominant negative (DN) mutants. Additionally, knock-down apoptosis signal-regulating kinase 1 (ASK1) by specific shRNA and blockade reactive oxygen species (ROS) by pharmacological inhibitor competently prevented β-Ecd-mediated inhibition of p38MAPK and ASK1 phosphorylation, respectively. These data provide the first evidence that β-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1–p38MAPK pathways. The neuroprotective effects of β-Ecd make it a promising candidate as a therapeutic agent for PD.
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