Overexpression of Circ_0005585 Alleviates Cerebral Ischemia Reperfusion Injury via Targeting MiR-16-5p.
Bull Exp Biol Med
; 175(3): 304-310, 2023 Jul.
Article
em En
| MEDLINE
| ID: mdl-37566250
ABSTRACT
Circular RNAs are implicated in the pathogenesis of ischemic stroke. In this work, we explored the modulation and potential mechanisms of action of circ_0005585 in ischemic stroke. Expression of circ_0005585 and miR-16-5p was assessed by quantitative real-time reverse transcription PCR. Ischemic stroke was modeled in mice by middle cerebral artery occlusion (MCAO). The infarct volume was assessed by triphenyl tetrazolium chloride staining. Neurological deficits were evaluated according to Neurological Severity Score. The permeability of the blood-brain barrier was assessed by Evan's blue leakage and brain water content. Apoptosis in brain tissues was measured by the TUNEL test. Relative expression of apoptosis-related proteins was evaluated by Western blotting. The direct interaction between circ_0005585 and miR-16-5p was verified by dual-luciferase reporter assay. The expression of circ_0005585 was lower in mice with MCAO. Lentivirus-mediated overexpression of circ_0005585 ameliorated the neurological deficits and decreased the infarction volume in MCAO mice. The brain water content and Evan's blue leakage through the blood-brain barrier were reduced. In addition, overexpression of circ_0005585 inhibited apoptosis in the cerebral tissues. Our results revealed direct interaction between circ_0005585 and miR-16-5p. Hence, circ_0005585 protects mouse brain during ischemic stroke by targeting miR-16-5p, which uncovers the pathogenesis of this pathology and opens new vitas for its therapy.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
6_ODS3_enfermedades_notrasmisibles
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão
/
Isquemia Encefálica
/
MicroRNAs
/
AVC Isquêmico
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Bull Exp Biol Med
Ano de publicação:
2023
Tipo de documento:
Article