Exosome-Derived lncRNA NEAT1 Exacerbates Sepsis-Associated Encephalopathy by Promoting Ferroptosis Through Regulating miR-9-5p/TFRC and GOT1 Axis

• DOI: 10.1007/s12035-022-02738-1
• Publication Date: 2022-01-17T08:23:58Z
• Authors: Xue-biao Wei; Wen-qiang Jiang; Ju-hao Zeng; Lin-qiang Huang; Hong-guang Ding; Yuan-wen Jing; Yong-li Han; Yi-chen Li; Sheng-long Chen
• Keywords: Exosome

Abstract Sepsis can cause sepsis-associated encephalopathy (SAE), but whether SAE was induced or exacerbated by ferroptosis remains unknown. In this study, the rat sepsis model constructed using cecal ligation and puncture method. The blood–brain barrier (BBB) permeability measured Evans blue dye (EBD) in vivo. levels of ROS, Fe ion, MDA, GSH, GPX4 were assessed enzyme-linked immunosorbent assay (ELISA). exosomes isolated from serum cultured with bEnd.3 cells for vitro analysis. Moreover, 100 μM FeCl3 (iron-rich) to simulate stress. cell viability evaluated Cell Counting Kit-8 (CCK-8) assay. A dual-luciferase reporter gene performed confirm relationship between miR-9-5p NEAT1, TFRC , GOT1 . vivo, it is found that BBB damaged rats. Level MDA increased, level GSH decreased, which means sepsis. Exosome-packaged NEAT1 significantly upregulated vitro, functions as a ceRNA facilitate expression. Overexpression enhanced stress cells. Increased alleviated sepsis-induced suppressing expression both vivo vitro. conclusion, these findings suggest high serous exosome-derived might exacerbate promoting through regulating miR-9-5p/ axis.