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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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We are analyzing https://link.springer.com/article/10.1007/s12035-014-8755-0.

Title:
Protective Effects of Salidroside in the MPTP/MPP+-Induced Model of Parkinson's Disease through ROS–NO-Related Mitochondrion Pathway | Molecular Neurobiology
Description:
Molecular Neurobiology - Parkinson
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {šŸ“}

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 {šŸ“ˆ}

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {šŸ’ø}

We see no obvious way the site makes money.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {šŸ”}

pubmed, article, google, scholar, cas, disease, parkinsons, salidroside, chen, oxidative, nitric, oxide, brain, wang, mitochondrial, res, dawson, zhang, stress, cells, neurodegeneration, pharmacol, alphasynuclein, cell, pathway, apoptosis, przedborski, model, dopaminergic, access, sci, central, med, mptp, jacksonlewis, privacy, cookies, content, protective, sal, neurons, reactive, species, toxicity, neurol, neurosci, death, information, publish, research,

Topics {āœ’ļø}

ask1-p38-nf-κb pathway month download article/chapter reducing α-synuclein aggregation interleukin-3-dependent haemopoietic cells sh-sy5y cells hydrogen peroxide-induced apoptosis ngf-differentiated pc-12 cells oxidative post-translational modifications parkinson patient-derived neurons reactive oxygen species 6-tetrahydropyridine-lesioned macaque model nerve growth factor full article pdf related mitochondrion pathway protect dopaminergic neurons mptp/mpp+-induced model human neuroblastoma cells apoptotic neuronal death reactive species formation aggregation exacerbates impairment mptp/mpp+-induced toxicity induced dopaminergic neurotoxicity privacy choices/manage cookies alpha-synuclein overexpression alpha-synuclein toxicity neuronal nitric oxide mpp+-induced apoptosis 6-ohda induced apoptosis related mitochondrial pathway cell damage induced related subjects nature science foundation progressive 1-methyl-4-phenyl-1 dose-dependent manner main active compound metal-induced toxicity intracellular free calcium 6-hydroxydopamine-induced neurodegeneration neurotoxin 1-methyl-4-phenyl-1 european economic area potent antioxidant properties beal mf green tea polyphenols chalmers-redman rm propargylamines induce antiapoptotic basal lipid peroxidation padovan-neto fe simbulan-rosenthal cm rat striatal synaptosomes traditional chinese medicine

Questions {ā“}

  • Maguire-Zeiss KA (2008) alpha-Synuclein: a therapeutic target for Parkinson's disease?
  • Maguire-Zeiss KA, Short DW, Federoff HJ (2005) Synuclein, dopamine and oxidative stress: co-conspirators in Parkinson's disease?

Schema {šŸ—ŗļø}

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         headline:Protective Effects of Salidroside in the MPTP/MPP+-Induced Model of Parkinson's Disease through ROS–NO-Related Mitochondrion Pathway
         description:Parkinson's disease is a progressive neurodegenerative disease causing tremor, rigidity, bradykinesia, and gait impairment. Oxidative stress and mitochondrial dysfunction play important roles in the development of Parkinson disease. Salidroside (Sal), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has potent antioxidant properties. Previous work from our group suggests that Sal might protect dopaminergic neurons through inhibition of reactive oxygen species (ROS) and nitric oxide (NO) generation. In the present study, we investigated the protective effects of Sal in MPTP/MPP+ models of Parkinson's disease in an attempt to elucidate the underlying mechanism of protection. We found that Sal pretreatment protected dopaminergic neurons against MPTP/MPP+-induced toxicity in a dose-dependent manner by: (1) reducing the production of ROS–NO, (2) regulating the ratio of Bcl-2/Bax, (3) decreasing cytochrome-c and Smac release, and inhibiting caspase-3, caspas-6, and caspas-9 activation, and (4) reducing α-synuclein aggregation. The present study supports the hypothesis that Sal may act as an effective neuroprotective agent through modulation of the ROS–NO-related mitochondrial pathway in vitro and in vivo.
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      headline:Protective Effects of Salidroside in the MPTP/MPP+-Induced Model of Parkinson's Disease through ROS–NO-Related Mitochondrion Pathway
      description:Parkinson's disease is a progressive neurodegenerative disease causing tremor, rigidity, bradykinesia, and gait impairment. Oxidative stress and mitochondrial dysfunction play important roles in the development of Parkinson disease. Salidroside (Sal), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has potent antioxidant properties. Previous work from our group suggests that Sal might protect dopaminergic neurons through inhibition of reactive oxygen species (ROS) and nitric oxide (NO) generation. In the present study, we investigated the protective effects of Sal in MPTP/MPP+ models of Parkinson's disease in an attempt to elucidate the underlying mechanism of protection. We found that Sal pretreatment protected dopaminergic neurons against MPTP/MPP+-induced toxicity in a dose-dependent manner by: (1) reducing the production of ROS–NO, (2) regulating the ratio of Bcl-2/Bax, (3) decreasing cytochrome-c and Smac release, and inhibiting caspase-3, caspas-6, and caspas-9 activation, and (4) reducing α-synuclein aggregation. The present study supports the hypothesis that Sal may act as an effective neuroprotective agent through modulation of the ROS–NO-related mitochondrial pathway in vitro and in vivo.
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External Links {šŸ”—}(216)

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