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• W4360878875 abstract "Acute liver failure (ALF) is a severe and potentially lethal clinical syndrome. It has been demonstrated that micro ribonucleic acids (miRNAs) are crucial mediators of nearly all pathological processes, including liver disease. The present study investigates the role of miR-378 in ALF. An ALF mouse model was induced using intraperitoneal injections of d-galactosamine/lipopolysaccharide (d-GalN/LPS). A hepatocyte cell line and miR-378 analogue were used in vitro to investigate the possible roles of miR-378 in ALF. The expressions of miR-378 and predicted target genes were measured via reverse transcription-quantitative polymerase chain reaction and western blotting, and cell apoptosis was assayed using flow cytometry. Compared with mice in the control group, the mice challenged with d-GalN/LPS showed higher levels of alanine aminotransferase, aspartate aminotransferase, tumour necrosis factor-alpha and interleukin-6, more severe liver damage and increased numbers of apoptotic hepatocytes. Hepatic miR-378 was distinctly downregulated, while messenger RNA and protein levels of cysteinyl aspartate specific proteinase 9 (caspase-9) were upregulated in the ALF model. Furthermore, miR-378 was downregulated in d-GalN/TNF-induced hepatocyte cells, and miR-378 was found to inhibit hepatocyte apoptosis by targeting caspase-9. Together, the present results indicate that miR-378 is a previously unrecognised post-ALF hepatocyte apoptosis regulator and may be a potential therapeutic target in the context of ALF. La insuficiencia hepática aguda (ALF) es un síndrome clínico grave y potencialmente letal. Se ha demostrado que los microácidos ribonucleicos (miRNA) son mediadores cruciales de casi todos los procesos patológicos, incluida la enfermedad hepática. El presente estudio investiga el papel de miR-378 en ALF. Se indujo ALF en un modelo de ratón usando inyecciones intraperitoneales de d-galactosamina/lipopolisacárido (d-GalN/LPS). Se utilizaron una línea celular de hepatocitos y un análogo de miR-378 in vitro para investigar las posibles funciones de miR-378 en ALF. Las expresiones de miR-378 y los genes diana predichos se midieron mediante la reacción en cadena de polimerasa cuantitativa con transcripción inversa y transferencia de Western, y la apoptosis celular se analizó mediante citometría de flujo. En comparación con los ratones del grupo de control, los ratones desafiados con d-GalN/LPS mostraron niveles más altos de alanina aminotransferasa, aspartato aminotransferasa, factor de necrosis tumoral alfa e interleucina-6, daño hepático más grave y un mayor número de hepatocitos apoptóticos. El miR-378 hepático se reguló claramente a la baja, mientras que el ARN mensajero y los niveles de proteína de la proteinasa 9 específica de aspartato de cisteinilo (caspasa-9) se regularon al alza en el modelo ALF. Además, miR-378 se reguló a la baja en las células de hepatocitos inducidas por d-GalN/TNF, y se descubrió que miR-378 inhibía la apoptosis de los hepatocitos al interferir en la transcripción de la caspasa-9. Juntos, los presentes resultados indican que miR-378 es un regulador de la apoptosis de hepatocitos post-ALF previamente no reconocido y puede ser un objetivo terapéutico potencial en el contexto de ALF." @default.
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• W4360878875 date "2023-02-01" @default.
• W4360878875 modified "2023-09-23" @default.
• W4360878875 title "MicroRNA-378 inhibits hepatocyte apoptosis during acute liver failure by targeting caspase-9 in mice" @default.
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• W4360878875 doi "https://doi.org/10.1016/j.gastre.2022.07.005" @default.
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