The neuroprotection of cerebrolysin after spontaneous intracerebral hemorrhage through regulates necroptosis via Akt/ GSK3B signaling pathway
Acta cir. bras
; Acta cir. bras;36(10): e361002, 2021. graf
Article
in En
| LILACS, VETINDEX
| ID: biblio-1349867
Responsible library:
BR1.1
ABSTRACT
ABSTRACT Purpose:
Spontaneous 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.Methods:
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. 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).Results:
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. The neuroprotective capacity of CBL is partly dependent on the Akt/GSK3β signaling pathway.Conclusions:
CBL improves neurological outcomes in mice and reduces neuronal death by protecting against neural necroptosis.Key words
Full text:
1
Collection:
01-internacional
Health context:
6_ODS3_enfermedades_notrasmisibles
Database:
LILACS
/
VETINDEX
Main subject:
Neuroprotective Agents
/
Necroptosis
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Acta cir. bras
Year:
2021
Document type:
Article