Exosomal miR‐122, miR‐128, miR‐200, miR‐298, and miR‐342 as novel diagnostic biomarkers in NAFL/NASH: Impact of LPS/TLR‐4/FoxO3 pathway

FOXO3公司 脂联素 非酒精性脂肪肝 脂肪肝 发病机制 肝硬化 小RNA 纤维化 癌症研究 生物 医学 内科学 免疫学 下调和上调 疾病 基因 胰岛素抵抗 遗传学 肥胖
作者
Ahmed Samy,Mohamed A. Kandeil,Dina Sabry,Ahmed A. Abdelghany,Mohamed O. Mahmoud
出处
期刊:Archiv Der Pharmazie [Wiley]
卷期号:357 (4) 被引量:5
标识
DOI:10.1002/ardp.202300631
摘要

Abstract Nonalcoholic fatty liver disease (NAFLD) is a common liver disorder affecting a quarter of the global residents. Progression of NAFL into nonalcoholic steatohepatitis (NASH) may cause cirrhosis, liver cancer, and failure. Gut microbiota imbalance causes microbial components translocation into the circulation, triggering liver inflammation and NASH‐related fibrosis. MicroRNAs (miRNAs) regulate gene expression via repressing target genes. Exosomal miRNAs are diagnostic and prognostic biomarkers for NAFL and NASH liver damage. Our work investigated the role of the gut microbiota in NAFLD pathogenesis via the lipopolysaccharide/toll‐like receptor 4/Forkhead box protein O3 (LPS/TLR‐4/FoxO3) pathway and certain miRNAs as noninvasive biomarkers for NAFL or its development to NASH. miRNA expression levels were measured using quantitative reverse transcription polymerase chain reaction (qRT‐PCR) in 50 NAFL patients, 50 NASH patients, and 50 normal controls. Plasma LPS, TLR‐4, adiponectin, peroxisome proliferator‐activated receptor γ (PPAR‐γ), and FoxO3 concentrations were measured using enzyme‐linked immunosorbent assay (ELISA). In NAFL and NASH patients, miR‐122, miR‐128, FoxO3, TLR‐4, LPS, and PPAR‐γ were upregulated while miR‐200, miR‐298, miR‐342, and adiponectin were downregulated compared with the normal control. The examined miRNAs might distinguish NAFL and NASH patients from the normal control using receiver operating characteristic analysis. Our study is the first to examine these miRNAs in NAFLD. Our findings imply that these are potentially promising biomarkers for noninvasive early NAFL diagnosis and NASH progression. Understanding the LPS/TLR‐4/FoxO3 pathway involvement in NAFL/NASH pathogenesis may aid disease management.
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