Long non-coding RNA LUCAT1 inhibits myocardial oxidative stress and apoptosis after myocardial infarction via targeting microRNA-181a-5p

This study hoped to explore the effects and mechanism of long non-coding RNA (lncRNA) LUCAT1 regulating microRNA-181a-5p (miR-181a-5p) on oxidative stress and apoptosis of cardiomyocytes induced by H(2)O(2). Totally, 72 patients with acute myocardial infarction (AMI) were included. H9c2 cardiomyocytes were cultured in vitro, and the H(2)O(2) model of cardiomyocytes was established. The expression levels of LUCAT1 and miR-181a-5p were detected by qRT-PCR after H(2)O(2) induction. The contents of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in cells were detected. The survival rate of the cells was detected by the Cell Counting Kit-8 (CCK-8) method; the apoptosis was detected by flow cytometry. The luciferase reporter experiment and quantitative real-time PCR (qRT-PCR) were used to verify the targeted relationship between LUCAT1 and miR-181a-5p. LUCAT1 was lowly expressed in the AMI patients. After H(2)O(2) induction, the expression of LUCAT1 in H9c2 cells lessened significantly, while the expression of miR-181a-5p elevated significantly (P < 0.001). Transfection of p-LUCAT1 significantly reversed the decreased SOD levels, the increased MDA and ROS content, and the elevated tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) in H(2)O(2)-stimulated cells (P < 0.001). Upregulation of LUCAT1 contributed to the mitigation of H(2)O(2) injury by promoting viable cells and repressing apoptotic cells (P < 0.01). LUCAT1 targeted miR-181a-5p and negatively regulated miR-181a-5p expression (P < 0.001). Collectively, LUCAT1 played a protective role on oxidative stress injury, inflammation, viability, and apoptosis of cardiomyocytes induced by H(2)O(2) via regulating miR-181a-5p.