Catalpol attenuates cardiomyocyte apoptosis in diabetic cardiomyopathy via Neat1/miR-140-5p/HDAC4 axis.

Catalpol attenuates cardiomyocyte apoptosis in diabetic cardiomyopathy via Neat1/miR-140-5p/HDAC4 axis. Biochimie. 2019 May 09;: Authors: Zou G, Zhong W, Wu F, Wang X, Liu L Abstract 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. PMID: 31078585 [PubMed - as supplied by publisher]
Source: Biochimie - Category: Biochemistry Authors: Tags: Biochimie Source Type: research