Abstract
Vitamin D deficiency is associated with acute myocardial infarction (AMI), thus we aimed to explore improvement effects of 1, 25-dihydroxyvitamin D3 (VD3) on the AMI and its potential mechanism. AMI models were constructed using male C57/BL6J mice and randomly treated with normal saline or VD3, using sham rats as control. Heart functions, myocardial damage, apoptosis and inflammation were evaluated. Cardiomyocytes isolated from 3-days-old suckling mice were used for in vitro verification. After VD3 treatment, AMI-induced cardiac dysfunction was reversed with better cardiac function parameters. VD3 treatment reduced inflammatory cell infiltration and myocardial infarction area accompanied by reduction of inflammatory factors and myocardial infarction markers compared to AMI group. VD3 treatment obviously alleviated AMI-induced myocardial apoptosis, along with Bcl-2 up-regulation and down-regulation of caspase-3, caspase-9 and Bax. Both in vivo and in vitro experiments revealed that VD3 enhanced expression of LC3II and Beclin-1 and decreased soluble p62. Furthermore, VD3 enhanced the AMI-caused inhibition of PI3K, p-AKT and p-mTOR expression, which was conversely reversed by addition of 3-methyladenine in vitro. The study highlights the improvement effects of VD3 on cardiac functions. We proposed a potential mechanism that VD3 protects against myocardial damage, inflammation and apoptosis by promoting autophagy through PI3K/AKT/mTOR pathway. This article is protected by copyright. All rights reserved.
Full text
