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Study · In vitro (cells) · 2013

7 results

Activation of AMP-activated protein kinase alleviates homocysteine-mediated neurotoxicity in SH-SY5Y cells.

Park YJ, Ko JW, Jang Y, Kwon YH

Neurochemical research27 Apr 2013Cited by 18 (Europe PMC)

PMID23624826 (opens in a new tab)DOI10.1007/s11064-013-1057-5 (opens in a new tab)PepBankPUB-23624826
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

7 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In SH-SY5Y cells, AICAR significantly protected against tunicamycin-induced cytotoxicity.

    In plain wordsIn cells, AICAR reduced tunicamycin-induced toxicity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTunicamycin-induced cytotoxicity
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment of SH-SY5Y human neuroblastoma cells with N (1)-(β-D-ribofuranosyl)-5-aminoimidazole-4-carboxamide (AICAR), a pharmacological activator of AMPK, significantly protected cells against cytotoxicity imposed by tunicamycin and homocysteine.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  2. 02LabIn vitro (cells)Mechanism

    In SH-SY5Y cells, AICAR significantly protected against homocysteine-induced cytotoxicity.

    In plain wordsIn cells, AICAR reduced homocysteine-induced toxicity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHomocysteine-induced cytotoxicity
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment of SH-SY5Y human neuroblastoma cells with N (1)-(β-D-ribofuranosyl)-5-aminoimidazole-4-carboxamide (AICAR), a pharmacological activator of AMPK, significantly protected cells against cytotoxicity imposed by tunicamycin and homocysteine.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  3. 03LabIn vitro (cells)Mechanism

    In SH-SY5Y cells, AICAR alleviated homocysteine-induced suppression of AMPK activation.

    In plain wordsIn cells, AICAR reduced homocysteine's suppression of AMPK activation.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAMPK activation
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Homocysteine significantly suppressed AMPK activation, which was alleviated by AICAR.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  4. 04LabIn vitro (cells)Mechanism

    In SH-SY5Y cells exposed to homocysteine, AICAR significantly inhibited the unfolded protein response.

    In plain wordsIn cells exposed to homocysteine, AICAR reduced the unfolded protein response.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseUnfolded protein response
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We observed a significant inhibition of the unfolded protein response by AICAR in cells incubated with homocysteine, suggesting a protective role of AMPK activation against ER stress-mediated neurotoxicity.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  5. 05LabIn vitro (cells)Mechanism

    In SH-SY5Y cells exposed to homocysteine, AICAR significantly reduced tau hyperphosphorylation.

    In plain wordsIn cells exposed to homocysteine, AICAR reduced excessive tau phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTau hyperphosphorylation
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR also significantly reduced tau hyperphosphorylation by inactivating glycogen synthase kinase-3β and c-Jun N-terminal kinase in cells incubated with homocysteine.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  6. 06LabIn vitro (cells)Mechanism

    In SH-SY5Y cells exposed to homocysteine, AICAR inactivated glycogen synthase kinase-3β.

    In plain wordsIn cells exposed to homocysteine, AICAR inactivated glycogen synthase kinase-3β.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseGlycogen synthase kinase-3β activity
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR also significantly reduced tau hyperphosphorylation by inactivating glycogen synthase kinase-3β and c-Jun N-terminal kinase in cells incubated with homocysteine.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.
  7. 07LabIn vitro (cells)Mechanism

    In SH-SY5Y cells exposed to homocysteine, AICAR inactivated c-Jun N-terminal kinase.

    In plain wordsIn cells exposed to homocysteine, AICAR inactivated c-Jun N-terminal kinase.

    Peptide
    AICAR (acadesine)
    Outcome
    Decreasec-Jun N-terminal kinase activity
    Study

    humann: not reported in source

    SH-SY5Y neuroblastoma cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR also significantly reduced tau hyperphosphorylation by inactivating glycogen synthase kinase-3β and c-Jun N-terminal kinase in cells incubated with homocysteine.
    1 context sentence
    Summary · context
    Therefore, we investigated whether AMPK activation alleviates ER stress-mediated neurotoxicity in SH-SY5Y human neuroblastoma cells incubated with homocysteine.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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