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Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. SNHG12 silencing enhanced the apoptosis of H/R-injured H9c2 cells, while SNHG12 overexpression relieved the cardiomyocyte apoptosis induced by H/R stimulation. Additionally, the suppression of SNHG12 significantly boosted the H/R-induced expression and the production of TNF-α, IL-6, and IL-1β, as well as the activation of NF-κB, which were fully reversed after overexpression of SNHG12. Mechanistically, SNHG12 adversely regulated the production of receptor for advanced glycation end products (RAGE) in H/R-stimulated H9c2 cells. Antibody blocking of RAGE alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have determined a valuable mechanism by which the high level of SNHG12 contributes to H9c2 cells against H/R injury through the reduction of RAGE expression.

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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.