The neuroprotection of cerebrolysin after spontaneous intracerebral hemorrhage through regulates necroptosis via Akt/ GSK3β signaling pathway.

Tao Y, Xu Y, Shen M, Feng X, Wu Y, Wu Y, Shen L, Wang Y

Acta cirurgica brasileira22 Nov 2021Cited by 5 (Europe PMC)

PMID34817023PMCIDPMC8610213DOI10.1590/acb361002PepBankPUB-34817023

Summary

PurposeSpontaneous intracerebral hemorrhage (ICH) is a major cause of death and disability with a huge economic burden worldwide. Cerebrolysin (CBL) has been previously used as a nootropic drug. Necroptosis is a programmed cell death mechanism that plays a vital role in neuronal cell death after ICH. However, the precise role of necroptosis in CBL neuroprotection following ICH has not been confirmed.MethodsIn the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model. Mortality, neurological score, brain water content, and neuronal death were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, Evans blue extravasation, Western blotting, and quantitative real-time polymerase chain reaction (PCR).ResultsThe results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH. The neuroprotective capacity of CBL is partly dependent on the Akt/GSK3β signaling pathway.ConclusionsCBL improves neurological outcomes in mice and reduces neuronal death by protecting against neural necroptosis.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with intracerebral hemorrhage, Cerebrolysin increased survival rate.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin increased survival.
Peptide
Cerebrolysin
Outcome
IncreaseSurvival rate
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Mortality · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702301
02AnimalAnimal study (in vivo)Efficacy outcome
In mice with intracerebral hemorrhage, Cerebrolysin increased neurological score.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin increased neurological score.
Peptide
Cerebrolysin
Outcome
IncreaseNeurological score
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702302
03AnimalAnimal study (in vivo)Efficacy outcome
In mice with intracerebral hemorrhage, Cerebrolysin increased neuron survival and reduced neuronal death.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin increased nerve cell survival.
Peptide
Cerebrolysin
Outcome
IncreaseNeuron survival
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702303
04AnimalAnimal study (in vivo)Mechanism
In mice with intracerebral hemorrhage, Cerebrolysin reduced RIP1 protein expression.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin reduced RIP1 protein expression.
Peptide
Cerebrolysin
Outcome
DecreaseRIP1 protein expression
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702304
05AnimalAnimal study (in vivo)Mechanism
In mice with intracerebral hemorrhage, Cerebrolysin reduced RIP3 protein expression.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin reduced RIP3 protein expression.
Peptide
Cerebrolysin
Outcome
DecreaseRIP3 protein expression
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702305
06AnimalAnimal study (in vivo)Mechanism
In mice with intracerebral hemorrhage, Cerebrolysin neuroprotection partly depended on Akt/GSK3β signaling.
In plain wordsIn mice with brain hemorrhage, Cerebrolysin protection partly depended on Akt/GSK3β signaling.
Peptide
Cerebrolysin
Outcome
Not applicableAkt/GSK3β pathway dependence
Study
micen: not reported in source
C57BL/6 mice with intracerebral hemorrhage
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
The neuroprotective capacity of CBL is partly dependent on the Akt/GSK3β signaling pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model.
Show in the study text Report a problemFND-3481702306

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.

Version 2Current
14 Oct 2026, 05:02 UTC
Study results updated
Version 1
14 Oct 2026, 01:46 UTC
First added · source update from Europe PMC

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