The protective role of microRNA-133b in restricting hippocampal neurons apoptosis and inflammatory injury in rats with depression by suppressing CTGF.
Int Immunopharmacol
; 78: 106076, 2020 Jan.
Article
en En
| MEDLINE
| ID: mdl-31830619
OBJECTIVE: Increasing evidence has proved the functions of microRNAs (miRNAs) in human diseases, our research was designed to explore the effects of miR-133b on the progression of depression with the involvement of connective tissue growth factor (CTGF). METHODS: Depression rat models were established by chronic unpredictable mild stress, then the ethology of rats in each group was observed, and the morphological changes as well as the apoptosis of hippocampal neurons was measured. Subsequently, the expression of miR-133b, CTGF, glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF), Bax, Bcl-2, interleukin-1ß (IL-1ß), IL-6, tumor necrosis factor-α (TNF-α) and neurotransmitters was determined. The target relation between miR-133b and CTGF was assessed. RESULTS: We have found in this study that miR-133b was poorly expressed, and CTGF was highly expressed in hippocampal tissues of depression rats. Additionally, elevated miR-133b and inhibited CTGF could restrain apoptosis of hippocampal neurons, repress inflammatory reaction, and increase the expression of GFAP, BDNF and neurotransmitters in hippocampal tissues of depression rats, resulting in a protective impact on neural injury in depression rats. CONCLUSION: This study demonstrates that elevated miR-133b could suppress the expression of CTGF to protect the hippocampal neurons from apoptosis and inflammatory injury in depression rats.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
MicroARNs
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Depresión
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Factor de Crecimiento del Tejido Conjuntivo
/
Hipocampo
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Inflamación
Tipo de estudio:
Prognostic_studies
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Int Immunopharmacol
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
FARMACOLOGIA
Año:
2020
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Países Bajos