Skip to content

Study · Animal study (in vivo) · rat · 2021

4 results

Brain Protein Expression Profile Confirms the Protective Effect of the ACTH(4-7)PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion.

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

International journal of molecular sciences8 Jun 2021Cited by 14 (Europe PMC)

PMID34201112 (opens in a new tab)PMCIDPMC8226508 (opens in a new tab)DOI10.3390/ijms22126179 (opens in a new tab)PepBankPUB-34201112
Download PDFPubMedAsk about this study
Jump to 4 results

Summary

The Semax (Met-Glu-His-Phe-Pro-Gly-Pro) peptide is a synthetic melanocortin derivative that is used in the treatment of ischemic stroke. Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription of neurotrophins and their receptors and modulated the expression of genes involved in the immune response. A genome-wide RNA-Seq analysis revealed that, in the rat transient middle cerebral artery occlusion (tMCAO) model, Semax suppressed the expression of inflammatory genes and activated the expression of neurotransmitter genes. Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke. At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax. Moreover, a regulatory network was constructed. In conclusion, the suppression of inflammatory and cell death processes and the activation of recovery may contribute to the neuroprotective action of Semax at both the transcriptome and protein levels.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In rats at 24 h after tMCAO, Semax upregulated active CREB in subcortical structures, including the ischemic focus.

    In plain wordsIn rats after stroke-like brain injury, Semax raised the level of the recovery protein CREB in deep brain areas.

    Peptide
    Semax
    Outcome
    IncreaseActive CREB in subcortical structures
    Study

    ratn: not reported in source

    transient middle cerebral artery occlusion (tMCAO) model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax.
    1 context sentence
    Summary · context
    Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In rats at 24 h after tMCAO, Semax downregulated MMP-9 in the adjacent frontoparietal cortex.

    In plain wordsIn rats after stroke-like brain injury, Semax lowered the level of the inflammation-related protein MMP-9 in nearby cortex.

    Peptide
    Semax
    Outcome
    DecreaseMMP-9 in adjacent frontoparietal cortex
    Study

    ratn: not reported in source

    transient middle cerebral artery occlusion (tMCAO) model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax.
    1 context sentence
    Summary · context
    Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In rats at 24 h after tMCAO, Semax downregulated c-Fos in the adjacent frontoparietal cortex.

    In plain wordsIn rats after stroke-like brain injury, Semax lowered the level of the protein c-Fos in nearby cortex.

    Peptide
    Semax
    Outcome
    Decreasec-Fos in adjacent frontoparietal cortex
    Study

    ratn: not reported in source

    transient middle cerebral artery occlusion (tMCAO) model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax.
    1 context sentence
    Summary · context
    Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In rats at 24 h after tMCAO, Semax downregulated active JNK in both tissues studied.

    In plain wordsIn rats after stroke-like brain injury, Semax lowered the level of the cell-death protein JNK in both brain areas.

    Peptide
    Semax
    Outcome
    DecreaseActive JNK in subcortical and cortical tissue
    Study

    ratn: not reported in source

    transient middle cerebral artery occlusion (tMCAO) model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax.
    1 context sentence
    Summary · context
    Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke.

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

    9 Oct 2026, 19:08 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.

PepBank is a research reference. Talk to a doctor before you use any peptide.