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Study · In vitro (cells) · 2025

3 results

Influence of Exogenous Neuropeptides on the Astrocyte Response Under Conditions of Continuous and Cyclic Hypoxia and Red Blood Cell Lysate.

Kojder K, Gąssowska-Dobrowolska M, Żwierełło W, Kłos P, Piotrowska K, Wszołek A, Maruszewska A, Gutowska I, Chlubek D, Baranowska-Bosiacka I

International journal of molecular sciences22 Apr 2025Cited by 2 (Europe PMC)

PMID40362194 (opens in a new tab)PMCIDPMC12071296 (opens in a new tab)DOI10.3390/ijms26093953 (opens in a new tab)PepBankPUB-40362194
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Summary

Acute brain injury includes different pathologies: stroke, traumatic injury, subarachnoidale haemorhhage. In the pathophysiology of acute brain injury, secondary injury with hyperactivation of glia plays a crucial role. Activated glial cells induce prolonged inflammation that impacts the recovery and further cognitive functions of patients. In our study, we have examined the neuroprotective impact of exogenous neuropeptides-Cerebrolysin on astrocytes under different conditions. In a model that simulates central nervous system damage associated with brain injury, stroke, and subarachnoid hemorrhage, the U87MG human brain cancer (glioblastoma astrocytoma like) cells were treated with Cerebrolysin and exposed to conditions of continuous and cyclic hypoxia and red blood cell lysate overload. The activity and expression of cyclooxygenases COX-1 and COX-2 and on cytokines (IL-8, IL-1β, IL-6, IL-10) and chemokines (CCL5/RANTES, CXCL9/MIG, CCL2/MCP-1, and CXCL10/IP-10) concentration were assessed. Cerebrolysin lowers IL-1β and IL-6 and increases IL-10 under all conditions. Cerebrolysin may exhibit a neuroimmunotrophic function, reducing inflammation under conditions that replicate traumatic brain injury and hemorrhagic insults to the central nervous system. By modulating both pro-inflammatory and anti-inflammatory cytokines, Cerebrolysin can help create a more balanced immune response conducive to tissue repair and reduced secondary damage. Its ability to lower harmful mediators like IL-1β and IL-6 while enhancing protective factors such as IL-10 suggests a promising therapeutic strategy in stroke, traumatic brain injury, and subarachnoid hemorrhage. Alongside other mechanisms such as neurotrophic factor enhancement and glial cell regulation, this cytokine modulation underscores the therapeutic potential of Cerebrolysin in a variety of central nervous system disorders.
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. 01LabIn vitro (cells)Mechanism

    In U87MG cells, Cerebrolysin lowered IL-1β under all tested conditions.

    In plain wordsIn cells, Cerebrolysin lowered IL-1β under all tested conditions.

    Peptide
    Cerebrolysin
    Outcome
    DecreaseIL-1β
    Study

    humann: not reported in source

    U87MG glioblastoma astrocytoma-like cells under continuous or cyclic hypoxia and red blood cell lysate overload
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cerebrolysin lowers IL-1β and IL-6 and increases IL-10 under all conditions.
    1 context sentence
    Summary · context
    In a model that simulates central nervous system damage associated with brain injury, stroke, and subarachnoid hemorrhage, the U87MG human brain cancer (glioblastoma astrocytoma like) cells were treated with Cerebrolysin and exposed to conditions of continuous and cyclic hypoxia and red blood cell lysate overload.
  2. 02LabIn vitro (cells)Mechanism

    In U87MG cells, Cerebrolysin lowered IL-6 under all tested conditions.

    In plain wordsIn cells, Cerebrolysin lowered IL-6 under all tested conditions.

    Peptide
    Cerebrolysin
    Outcome
    DecreaseIL-6
    Study

    humann: not reported in source

    U87MG glioblastoma astrocytoma-like cells under continuous or cyclic hypoxia and red blood cell lysate overload
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cerebrolysin lowers IL-1β and IL-6 and increases IL-10 under all conditions.
    1 context sentence
    Summary · context
    In a model that simulates central nervous system damage associated with brain injury, stroke, and subarachnoid hemorrhage, the U87MG human brain cancer (glioblastoma astrocytoma like) cells were treated with Cerebrolysin and exposed to conditions of continuous and cyclic hypoxia and red blood cell lysate overload.
  3. 03LabIn vitro (cells)Mechanism

    In U87MG cells, Cerebrolysin increased IL-10 under all tested conditions.

    In plain wordsIn cells, Cerebrolysin increased IL-10 under all tested conditions.

    Peptide
    Cerebrolysin
    Outcome
    IncreaseIL-10
    Study

    humann: not reported in source

    U87MG glioblastoma astrocytoma-like cells under continuous or cyclic hypoxia and red blood cell lysate overload
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cerebrolysin lowers IL-1β and IL-6 and increases IL-10 under all conditions.
    1 context sentence
    Summary · context
    In a model that simulates central nervous system damage associated with brain injury, stroke, and subarachnoid hemorrhage, the U87MG human brain cancer (glioblastoma astrocytoma like) cells were treated with Cerebrolysin and exposed to conditions of continuous and cyclic hypoxia and red blood cell lysate overload.

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

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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