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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

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 {🗺️}

WebPage:
      mainEntity:
         headline:β-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38MAPK–p53 Signaling Pathway
         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.
         datePublished:2016-05-26T00:00:00Z
         dateModified:2016-05-26T00:00:00Z
         pageStart:453
         pageEnd:466
         sameAs:https://doi.org/10.1007/s12640-016-9631-7
         keywords:
            β-Ecdysterone
            Parkinson’s disease
            p38MAPK
            Apoptosis
            Mitochondrial membrane potential
            Neurosciences
            Neurology
            Neurochemistry
            Pharmacology/Toxicology
            Neurobiology
            Cell Biology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig6_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig7_HTML.gif
         isPartOf:
            name:Neurotoxicity Research
            issn:
               1476-3524
               1029-8428
            volumeNumber:30
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Zhi Pan
               affiliation:
                     name:Changchun University of Chinese Medicine
                     address:
                        name:Center for New Medicine Research, Changchun University of Chinese Medicine, Changchun, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Yingcai Niu
               affiliation:
                     name:Qiqihar Medical University
                     address:
                        name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Yini Liang
               affiliation:
                     name:Qiqihar Medical University
                     address:
                        name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Xiaojie Zhang
               affiliation:
                     name:Qiqihar Medical University
                     address:
                        name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Miaoxian Dong
               affiliation:
                     name:Qiqihar Medical University
                     address:
                        name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:β-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38MAPK–p53 Signaling Pathway
      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.
      datePublished:2016-05-26T00:00:00Z
      dateModified:2016-05-26T00:00:00Z
      pageStart:453
      pageEnd:466
      sameAs:https://doi.org/10.1007/s12640-016-9631-7
      keywords:
         β-Ecdysterone
         Parkinson’s disease
         p38MAPK
         Apoptosis
         Mitochondrial membrane potential
         Neurosciences
         Neurology
         Neurochemistry
         Pharmacology/Toxicology
         Neurobiology
         Cell Biology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig6_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12640-016-9631-7/MediaObjects/12640_2016_9631_Fig7_HTML.gif
      isPartOf:
         name:Neurotoxicity Research
         issn:
            1476-3524
            1029-8428
         volumeNumber:30
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Zhi Pan
            affiliation:
                  name:Changchun University of Chinese Medicine
                  address:
                     name:Center for New Medicine Research, Changchun University of Chinese Medicine, Changchun, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yingcai Niu
            affiliation:
                  name:Qiqihar Medical University
                  address:
                     name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yini Liang
            affiliation:
                  name:Qiqihar Medical University
                  address:
                     name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Xiaojie Zhang
            affiliation:
                  name:Qiqihar Medical University
                  address:
                     name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Miaoxian Dong
            affiliation:
                  name:Qiqihar Medical University
                  address:
                     name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Neurotoxicity Research
      issn:
         1476-3524
         1029-8428
      volumeNumber:30
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Changchun University of Chinese Medicine
      address:
         name:Center for New Medicine Research, Changchun University of Chinese Medicine, Changchun, China
         type:PostalAddress
      name:Qiqihar Medical University
      address:
         name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
         type:PostalAddress
      name:Qiqihar Medical University
      address:
         name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
         type:PostalAddress
      name:Qiqihar Medical University
      address:
         name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
         type:PostalAddress
      name:Qiqihar Medical University
      address:
         name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Zhi Pan
      affiliation:
            name:Changchun University of Chinese Medicine
            address:
               name:Center for New Medicine Research, Changchun University of Chinese Medicine, Changchun, China
               type:PostalAddress
            type:Organization
      name:Yingcai Niu
      affiliation:
            name:Qiqihar Medical University
            address:
               name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
               type:PostalAddress
            type:Organization
      name:Yini Liang
      affiliation:
            name:Qiqihar Medical University
            address:
               name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
               type:PostalAddress
            type:Organization
      name:Xiaojie Zhang
      affiliation:
            name:Qiqihar Medical University
            address:
               name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
               type:PostalAddress
            type:Organization
      name:Miaoxian Dong
      affiliation:
            name:Qiqihar Medical University
            address:
               name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Center for New Medicine Research, Changchun University of Chinese Medicine, Changchun, China
      name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
      name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
      name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
      name:The Institute of Medicine, Qiqihar Medical University, Qiqihar, China
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(175)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

3.73s.

LINK . SPRINGER . COM {}