| First Author | Zou G | Year | 2019 |
| Journal | Cell Cycle | Volume | 18 |
| Issue | 24 | Pages | 3432-3441 |
| PubMed ID | 31736383 | Mgi Jnum | J:298411 |
| Mgi Id | MGI:6480088 | Doi | 10.1080/15384101.2019.1673619 |
| Citation | Zou G, et al. (2019) Inhibition of lncRNA Neat1 by catalpol via suppressing transcriptional activity of NF-kappaB attenuates cardiomyocyte apoptosis. Cell Cycle 18(24):3432-3441 |
| abstractText | 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 IkappaBalpha and the nuclear localization of nulear factor-kappaB (NF-kappaB) by decreasing the intracellular ROS levels. Additionally, chromatin immunoprecipitation (ChIP) and dual-luciferase activity assays validated that NF-kappaB 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-kappaB-Neat1 axis. |
