期刊
AGING-US
卷 12, 期 10, 页码 9066-9084出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.103172
关键词
non-alcoholic steatohepatitis; miR142-5p; TSLP; JAK-STAT signaling pathway
资金
- National Key Specialty Construction Project of Clinical Pharmacy [3030503069]
- Research Fund for the Doctoral Program of Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital [30305030843P]
This study aimed to figure out the underlying mechanism of miR-142-5p in the non-alcoholic steatohepatitis (NASH). Bioinformatics, luciferase assay and Western blot were performed. The NASH mouse model was established through feeding a high fat diet (HFD). Relative expressions of miR-142-5p, thymic stromal lymphopoietin (TSLP), inflammatory factors were detected by qRT-PCR. The injury level of liver was assessed via measurement of serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). H&E staining and Masson's trichrome staining examine the liver fatty degeneration and fibrosis. MiR-142-5p and TSLP were differentially expressed and JAK-STAT signaling pathway was activated in the NASH group. Luciferase assay identified that TSLP was the downstream target of miR-142-5p. Through overexpression of miR-142-5p, ALT and AST in serum were inhibited, pro-inflammatory factors, liver fatty degeneration and fibrosis in liver tissues were decreased, while anti-inflammatory factors were increased. Overexpression of TSLP and JAK-STAT signaling pathway activation could reverse the effects of miR-142-5p on NASH. Taken together, overexpression of miR-142-5p could attenuate NASH progression via inhibiting TSLP and JAK-STAT pathway. MiR-142-5p might be a novel latent target for NASH therapy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据