期刊
BIOCHIMIE
卷 165, 期 -, 页码 90-99出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2019.05.005
关键词
Catalpol; Cardiomyocyte apoptosis; Diabetic cardiomyopathy; HDAC4; Neat1
资金
- Supporting Plan for Excellent Innovative Talents of Heilongjiang University of Traditional Chinese Medicine
- Heilongjiang Post-doctoral Research Initiation Fund
- Two-class and Superiority Discipline Construction Project [051022]
The cardioprotection of catalpol and its mechanism in diabetic cardiomyopathy (DCM) remains unclear. Here, mouse cardiomyocytes were treated with high glucose (HG) to establish a model of cellular injury induced by HG. In vitro experiments were carried out and confirmed that Catalpol attenuated HG-induced long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (Neat1) expression in mouse cardiomyocytes. Mechanistically, luciferase reporter analysis indicated that Neat1 could decrease the transcription of miR-140-5p to positively regulate histone deacetylase 4 (HDAC4) expression. Notably, overexpression of miR-140-5p or silencing of HDAC4 rescued Neat1-induced cardiomyocyte apoptosis. DCM was induced in male C57BL/6 mice by intraperitoneal injection with streptozotocin (STZ) combined with a high-fat/high-sugar diet. Further in vivo experiments identified that Catalpol alleviated myocardial damage by regulating Neat1/miR-140-5p/HDAC4 axis in DCM mice. Thus, our results demonstrated that Catalpol could exert cardioprotective effect against DCM via Neat1/ miR-140-5p/HDAC4 pathway. (C) 2019 Published by Elsevier B.V.
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