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Study · In vitro (cells) · 2014

5 results

Activation of AMPK attenuates lipopolysaccharide-impaired integrity and function of blood-brain barrier in human brain microvascular endothelial cells.

Zhao Z, Hu J, Gao X, Liang H, Liu Z

Experimental and molecular pathology16 Sept 2014Cited by 60 (Europe PMC)

PMID25220346 (opens in a new tab)DOI10.1016/j.yexmp.2014.09.006 (opens in a new tab)PepBankPUB-25220346
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 study5

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

  1. 01LabIn vitro (cells)Mechanism

    In human brain endothelial cells, AICAR reversed LPS-induced elevation of barrier permeability.

    In plain wordsIn cells, AICAR reversed the increase in brain barrier permeability caused by LPS.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseBlood-brain barrier permeability
    Study

    humann: not reported in source

    LPS-exposed human brain microvascular endothelial cells
    Comparator
    LPS alone
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All effects induced by LPS in HBVMCs were reversed by adenoviral overexpression of superoxide dismutase, inhibition of NAD(P)H oxidase by apocynin or gain-function of AMPK by adenoviral overexpression of constitutively active mutant (AMPK-CA) or by 5-amino-4-imidazole carboxamide riboside (AICAR).
    1 context sentence
    Summary · context
    The exposure of human brain microvascular endothelial cells (HBMECs) to LPS (1 μg/ml) for 4 to 24h a week dramatically increased the permeability of the BBB in parallel with the lowered expression levels of occludin and claudin-5, which are essential to maintain tight junctions in HBMECs.
  2. 02LabIn vitro (cells)Mechanism

    In human brain endothelial cells, AICAR reversed the LPS-induced reduction in occludin expression.

    In plain wordsIn cells, AICAR reversed the reduction in occludin caused by LPS.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseOccludin expression
    Study

    humann: not reported in source

    LPS-exposed human brain microvascular endothelial cells
    Comparator
    LPS alone
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All effects induced by LPS in HBVMCs were reversed by adenoviral overexpression of superoxide dismutase, inhibition of NAD(P)H oxidase by apocynin or gain-function of AMPK by adenoviral overexpression of constitutively active mutant (AMPK-CA) or by 5-amino-4-imidazole carboxamide riboside (AICAR).
    1 context sentence
    Summary · context
    The exposure of human brain microvascular endothelial cells (HBMECs) to LPS (1 μg/ml) for 4 to 24h a week dramatically increased the permeability of the BBB in parallel with the lowered expression levels of occludin and claudin-5, which are essential to maintain tight junctions in HBMECs.
  3. 03LabIn vitro (cells)Mechanism

    In human brain endothelial cells, AICAR reversed the LPS-induced reduction in claudin-5 expression.

    In plain wordsIn cells, AICAR reversed the reduction in claudin-5 caused by LPS.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseClaudin-5 expression
    Study

    humann: not reported in source

    LPS-exposed human brain microvascular endothelial cells
    Comparator
    LPS alone
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All effects induced by LPS in HBVMCs were reversed by adenoviral overexpression of superoxide dismutase, inhibition of NAD(P)H oxidase by apocynin or gain-function of AMPK by adenoviral overexpression of constitutively active mutant (AMPK-CA) or by 5-amino-4-imidazole carboxamide riboside (AICAR).
    1 context sentence
    Summary · context
    The exposure of human brain microvascular endothelial cells (HBMECs) to LPS (1 μg/ml) for 4 to 24h a week dramatically increased the permeability of the BBB in parallel with the lowered expression levels of occludin and claudin-5, which are essential to maintain tight junctions in HBMECs.
  4. 04LabIn vitro (cells)Mechanism

    In human brain endothelial cells, AICAR reversed the LPS-induced increase in reactive oxygen species production.

    In plain wordsIn cells, AICAR reversed the rise in reactive oxygen molecules caused by LPS.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseReactive oxygen species production
    Study

    humann: not reported in source

    LPS-exposed human brain microvascular endothelial cells
    Comparator
    LPS alone
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All effects induced by LPS in HBVMCs were reversed by adenoviral overexpression of superoxide dismutase, inhibition of NAD(P)H oxidase by apocynin or gain-function of AMPK by adenoviral overexpression of constitutively active mutant (AMPK-CA) or by 5-amino-4-imidazole carboxamide riboside (AICAR).
    1 context sentence
    Summary · context
    In addition, LPS significantly increased the reactive oxygen species (ROS) productions.
  5. 05LabIn vitro (cells)Mechanism

    In human brain endothelial cells, AICAR abolished the LPS-enhanced levels of NAD(P)H oxidase subunit proteins.

    In plain wordsIn cells, AICAR blocked the increase in NAD(P)H oxidase proteins caused by LPS.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNAD(P)H oxidase subunit protein expression
    Study

    humann: not reported in source

    LPS-exposed human brain microvascular endothelial cells
    Comparator
    LPS alone
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Finally, the upregulation of AMPK by either AMPK-CA or AICAR abolished the levels of LPS-enhanced NAD(P)H oxidase subunit protein expressions.
    1 context sentence
    Summary · context
    All effects induced by LPS in HBVMCs were reversed by adenoviral overexpression of superoxide dismutase, inhibition of NAD(P)H oxidase by apocynin or gain-function of AMPK by adenoviral overexpression of constitutively active mutant (AMPK-CA) or by 5-amino-4-imidazole carboxamide riboside (AICAR).

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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