Silencing of Long Noncoding RNA MIAT Contributes to Relieving Sepsis-Induced Myocardial Depression via the NF-κB Axis.
J Surg Res
; 278: 282-292, 2022 10.
Article
en En
| MEDLINE
| ID: mdl-35636204
ABSTRACT
INTRODUCTION:
Sepsis represents a life-threatening disease caused by a series of infections, which may be complicated with severe myocardial depression (MD). Long noncoding RNAs (lncRNAs) are closely related to sepsis-induced myocardial depression (SIMD). This study aimed to seek out the mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in the growth of SIMD.METHODS:
Venous blood samples were collected from 62 patients with sepsis; the sepsis rat model was established with 15 mg/kg lipopolysaccharide (LPS), and the H9C2 cardiomyocyte injury model was established with 1 µg/mL LPS. In the rat and cardiomyocyte models, MIAT was inhibited. The expression of MIAT in normal tissues and SIMD tissues was detected. Then, the functional assays of MIAT were performed in rats and H9C2 cells for detection of cardiac function, hemodynamics, inflammation response, myocardial function, oxidative stress, tissue stainings, and cardiomyocyte viability and apoptosis. Western blot analysis was used to measure the levels of apoptosis-related proteins and the nuclear factor kappa B (NF-κB) axis-related proteins.RESULTS:
MIAT was highly expressed in SIMD patients. Silencing MIAT alleviated inflammation and apoptosis and improved myocardial function in SIMD rats by downregulating the NF-κB axis. In LPS-induced H9C2 cardiomyocytes, silencing MIAT alleviated inflammation and oxidative stress and inhibited apoptosis by downregulating the NF-κB axis, thus mitigating cardiomyocyte injury.CONCLUSIONS:
MIAT could assist the diagnosis of SIMD and might affect the progression of SIMD by regulating the NF-κB pathway.Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Sepsis
/
MicroARNs
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ARN Largo no Codificante
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Cardiomiopatías
/
Infarto del Miocardio
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Surg Res
Año:
2022
Tipo del documento:
Article
País de afiliación:
China