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논문 기본 정보

자료유형
학술저널
저자정보
Gang Xu (Department of Laboratory Medicine the First Affiliated Hospital of Wenzhou Medical University) Yu-Min Wang (Department of Laboratory Medicine the First Affiliated Hospital of Wenzhou Medical University) Miao-Miao Ying (Department of Pathology the First Affiliated Hospital of Wenzhou Medical University) Sui-Dan Chen (Department of Pathology the First Affiliated Hospital of Wenzhou Medical University) Zong-Rui Li (School of Basic Medical Sciences Shanghai Medical College Fudan University) Hong-Lei Ma (Department of Hepatology the First Affiliated Hospital of Wenzhou Medical University) Ming-Hua Zheng (Department of Hepatology the First Affiliated Hospital of Wenzhou Medical University) Jian Wu (Department of Gastroenterology & Hepatology Zhongshan Hospital of Fudan University) Chunming Ding (School of Laboratory Medicine and Life Science Wenzhou Medical University)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology 제27권 제2호
발행연도
2021.1
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329 - 345 (17page)

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Background/Aims: Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis. We aimed to investigate the usefulness of a key biomarker, lipocalin-2 (LCN2), for the detection of NASH progression. Methods: A mouse NASH model was established using a high-fat diet and a high-sugar drinking water. Gene expression profile of the NASH model was analyzed using RNA sequencing. Moreover, 360 NAFLD patients (steatosis, 83; NASH, 277), 40 healthy individuals, and 87 patients with alcoholic fatty liver disease were recruited. Results: Inflammatory infiltration, focal necrosis in the leaflets, steatosis, and fibrosis were documented in the mouse liver. In total, 504 genes were differentially expressed in the livers of NASH mice, and showed significant functional enrichment in the inflammation-related category. Upregulated liver LCN2 was found to be significantly interactive with various interleukins and toll-like receptors. Serum LCN2 levels were significantly increased in NAFLD patients. Serum LCN2 levels were correlated with steatosis, intralobular inflammation, semiquantitative fibrosis score, and nonalcoholic fatty liver disease activity score. The area under the curve of serum LCN2 was 0.987 with a specificity of 100% and a sensitivity of 93.5% for NASH diagnosis, and 0.977 with almost the same specificity and sensitivity for steatosis. Conclusions: LCN2 might be involved in the transition from NAFL to NASH by mediating inflammation. Serum LCN2 levels might be a novel biomarker for the diagnosis of NASH.

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