Long Non-Coding RNA SNHG8 Plays a Key Role in Myocardial Infarction Through Affecting Hypoxia-Induced Cardiomyocyte Injury.

Abstract

BackgroundThe objective of the study was to explore the role of long non-coding RNA SNHG8 (lncRNA SNHG8) in myocardial infarction (MI) and the related mechanism of action.Material/MethodsIn vitro model of MI was established by hypoxia induction in cardiomyocyte line H9c2 cells. H9c2 cells were transfected with control-plasmid, SNHG8-plasmid, control-shRNA and SNHG8-shRNA. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed to measure transfection efficiency. Creatine kinase-muscle/brain (CK-MB) release, cardiac troponin 1 (cTnI) release and mitochondria viability were detected by using related detection kits. MTT (3-(45)-dimethylthiahiazo (-z-y 1)-35-diphenytetrazoliumromide) assay was used to detect cell viability and flow cytometry analysis was used to detect cell apoptosis. Western blot assay was performed to measure protein expression of cleaved-Caspase3, p-p65 and p65. Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR assay were performed to detect expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6.ResultsLncRNA SNHG8 was overexpressed in hypoxia-induced cardiomyocytes. SNHG8-plasmid increased lncRNA SNHG8 expression, CK-MB release, cTnI release, and mitochondria viability in hypoxia-induced H9c2 cells. In addition, SNHG8-plasmid reduced cell viability, induced cell apoptosis, and increased expression of cleaved-caspase3, IL-1β, TNF-α, IL-6, and p-p65 in hypoxia-induced H9c2 cells, while the effects of SNHG8-shRNA were opposite.ConclusionsWe demonstrated that lncRNA SNHG8 affected myocardial infarction by affecting hypoxia-induced cardiomyocyte injury via regulation of the NF-κB pathway.