Effects of long non-coding RNA NEAT1 on sepsis-induced brain injury in mice via NF-κB.
Eur Rev Med Pharmacol Sci
; 23(9): 3933-3939, 2019 May.
Article
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| MEDLINE
| ID: mdl-31115021
ABSTRACT
OBJECTIVE:
The aim of this study was to investigate the effect of long non-coding ribonucleic acid (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) on sepsis-induced brain injury in mice through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). MATERIALS ANDMETHODS:
The mouse model of sepsis was established by cecal ligation and puncture induction. The relative expression levels of NEAT1 and NF-κB in brain tissues of mice in healthy group and sepsis group were determined via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting, respectively. Subsequently, the expression of NEAT1 was silenced by transfection of small interfering RNAs (siRNAs). Meanwhile, its effect on NF-κB expression was detected. To further explore the effect of sepsis on brain injury, the content of brain water and the expression levels of apoptosis-related proteins, including B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (BAX), in mice of healthy group, sepsis group, and sepsis + si-NEAT1 group were measured. Furthermore, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were used to detect the proliferation and apoptosis of nerve cells.RESULTS:
The relative expression levels of NEAT1 and NF-κB were significantly increased in the brain tissues of septic mice (p<0.01). Si-NEAT1 transfection significantly decreased the expressions of NEAT1 and NF-κB in brain tissues of septic mice (p<0.05). The content of brain water in mice of sepsis group was evidently increased (p<0.05). However, si-NEAT1 treatment remarkably reduced this content (p<0.05). In addition, sepsis markedly decreased the activity of nerve cells (p<0.05). However, si-NEAT1 could significantly increase the activity of nerve cells in septic mice (p<0.05). Moreover, si-NEAT1 notably decreased the expression of BAX (p<0.05), whereas it increased the expression of Bcl-2 (p<0.05). The results of apoptosis detection revealed that sepsis remarkably promoted the apoptosis of mouse nerve cells (p<0.05). In addition, si-NEAT1 transfection could evidently alleviate the apoptosis of nerve cells in septic mice (p<0.05).CONCLUSIONS:
LncRNA NEAT1 promotes brain injury in septic mice by positively regulating NF-κB. However, si-NEAT1 transfection can reduce this injury.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Lesiones Encefálicas
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FN-kappa B
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Sepsis
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ARN Largo no Codificante
Tipo de estudio:
Etiology_studies
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Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Asunto de la revista:
FARMACOLOGIA
/
TOXICOLOGIA
Año:
2019
Tipo del documento:
Article
País de afiliación:
China