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Study · Animal study (in vivo) · rat · 2020

3 results

Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats.

Filippenkov IB, Stavchansky VV, Denisova AE, Yuzhakov VV, Sevan'kaeva LE, Sudarkina OY, Dmitrieva VG, Gubsky LV, Myasoedov NF, Limborska SA, Dergunova LV

Genes22 Jun 2020Cited by 24 (Europe PMC)

PMID32580520 (opens in a new tab)PMCIDPMC7350263 (opens in a new tab)DOI10.3390/genes11060681 (opens in a new tab)PepBankPUB-32580520
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Summary

Cerebral ischaemia is the most common cause of impaired brain function. Biologically active peptides represent potential drugs for reducing the damage that occurs after ischaemia. The synthetic melanocortin derivative, ACTH(4-7)PGP (Semax), has been used successfully in the treatment of patients with severe impairment of cerebral blood circulation. However, its molecular mechanisms of action within the brain are not yet fully understood. Previously, we used the transient middle cerebral artery occlusion (tMCAO) model to study the damaging effects of ischaemia-reperfusion on the brain transcriptome in rats. Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions. We have identified 394 differentially expressed genes (DEGs) (>1.5-fold change) in the brains of rats at 24 h after tMCAO treated with Semax relative to saline. Following tMCAO, we found that Semax suppressed the expression of genes related to inflammatory processes and activated the expression of genes related to neurotransmission. In contrast, ischaemia-reperfusion alone activated the expression of inflammation-related genes and suppressed the expression of neurotransmission-related genes. Therefore, the neuroprotective action of Semax may be associated with a compensation of mRNA expression patterns that are disrupted during ischaemia-reperfusion conditions.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In rats 24 h after transient middle cerebral artery occlusion, Semax treatment changed the expression of 394 genes compared with saline.

    In plain wordsIn rats after an induced stroke, Semax changed the activity of 394 brain genes compared with saline.

    Peptide
    Semax
    Outcome
    Not applicableDifferentially expressed genes with Semax versus saline
    Study

    ratn: not reported in source

    tMCAO ischaemia-reperfusion, brain at 24 h
    Comparator
    Saline
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Measurements

    Differentially expressed genes
    394 genes
    Semax versus saline, 24 h after tMCAO

    Source sentences

    Summary
    We have identified 394 differentially expressed genes (DEGs) (>1.5-fold change) in the brains of rats at 24 h after tMCAO treated with Semax relative to saline.
    1 context sentence
    Summary · context
    Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In rats after transient middle cerebral artery occlusion, Semax suppressed the expression of genes related to inflammatory processes.

    In plain wordsIn rats after an induced stroke, Semax lowered the activity of genes linked to inflammation.

    Peptide
    Semax
    Outcome
    DecreaseInflammation-related gene expression
    Study

    ratn: not reported in source

    tMCAO ischaemia-reperfusion, brain at 24 h
    Comparator
    Saline
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Semax suppressed the expression of genes related to inflammatory processes and activated the expression of genes related to neurotransmission.
    1 context sentence
    Summary · context
    Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In rats after transient middle cerebral artery occlusion, Semax activated the expression of genes related to neurotransmission.

    In plain wordsIn rats after an induced stroke, Semax raised the activity of genes linked to nerve signaling.

    Peptide
    Semax
    Outcome
    IncreaseNeurotransmission-related gene expression
    Study

    ratn: not reported in source

    tMCAO ischaemia-reperfusion, brain at 24 h
    Comparator
    Saline
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    activated the expression of genes related to neurotransmission.
    1 context sentence
    Summary · context
    Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions.

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

    10 Oct 2026, 10:21 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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