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• W2892268959 abstract "Rapid and accurate diagnosis of neonatal sepsis (NS) is highly warranted because of high associated morbidity and mortality. The study aims to evaluate the effects of miR-300 on inflammatory responses in a septic neonate mouse model.A septic mouse model was established by intraperitoneal (i.p.) cecal slurry (CS) injection in order to validate the effect of miR-300 on the inflammatory response in endothelial cells. Bioinformatics tools and luciferase activity were employed to detect the target of miR-300. Serum inflammatory factors were determined by ELISA assay. RT-qPCR and western blot analysis were used to determine the gene expressions. Flow cytometry was employed to evaluate cell apoptosis.Gain- and loss-of-function studies revealed that miR-300 overexpression augmented autophagy, inhibited cell apoptosis, enhanced cell cycle entry in endothelial cells, and decreased inflammatory response through the regulation of pro- and anti-apoptotic factors in endothelial cells. The effect of miR-300on endothelial cells was upregulated after nicotinamide phosphoribosyltransferase (NAMPT) silencing and AMPK/mTOR signaling pathway activation, indicating that miR-300 influences sepsis via suppressing NAMPT and triggering the AMPK/mTOR signaling pathway.Our study provides evidence indicating that overexpressedmiR-300 enhances autophagy by targeting NAMPT through activation of the AMPK/mTOR signaling pathway in septic mouse models, indicating it may serve as a potential therapeutic target for sepsis." @default.
• W2892268959 created "2018-09-27" @default.
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• W2892268959 date "2018-12-01" @default.
• W2892268959 modified "2023-10-16" @default.
• W2892268959 title "microRNA-300/NAMPT regulates inflammatory responses through activation of AMPK/mTOR signaling pathway in neonatal sepsis" @default.
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• W2892268959 doi "https://doi.org/10.1016/j.biopha.2018.08.064" @default.
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