Inhibition of lncRNA Neat1 by catalpol via suppressing transcriptional activity of NF-κB attenuates cardiomyocyte apoptosis. Issue 24 (17th December 2019)

• Record Type: Journal Article
• Authors: Zou, Guoliang; Zhong, Weili; Wu, Fan; Wang, Xiaoxue; Liu, Li
• Is Part Of: Cell cycle. Volume 18:Issue 24(2019)
• Page Start: 3432
• Page End: 3441
• Publication Date: 2019-12-17
• Subjects: Cardiomyocytes -- Catalpol -- Neat1 -- NF-κB -- oxidative stress; Cell cycle -- Periodicals; 571.84377
• DOI: 10.1080/15384101.2019.1673619
• Languages: English
• ISSNs: 1538-4101

Abstract

ABSTRACT: Oxidative stress is considered as a major pathogenesis in myocardial damage; however, effective therapies are limited so far. The present study aimed to investigate the in vitro antioxidative mechanism of Catalpol in cardiomyocytes. The results indicated that Catalpol attenuated high glucose (HG)-induced apoptosis in mouse cardiomyocytes via significantly downregulating long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (Neat1) expression. Furthermore, Catalpol downregulated Neat1 expression and attenuated apoptosis by inhibiting production of intracellular reactive oxygen species (ROS) in HG-treated cardiomyocytes. Moreover, Catalpol also suppressed HG-induced degradation of IκBα and the nuclear localization of nulear factor-κB (NF-κB) by decreasing the intracellular ROS levels. Additionally, chromatin immunoprecipitation (ChIP) and dual-luciferase activity assays validated that NF-κB bound to Neat1 promoter to activate Neat1 expression. In summary, these results implied that Catalpol protected mouse cardiomyocytes against oxidative injury at least partly through ROS-NF-κB-Neat1 axis.