Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression

Abstract

Long non-coding (lnc)RNAs serve a role in a number of diseases, including different types of cancer and acute myocardial infarction. The aim of the present study was to investigate the protective role of lncRNA small nucleolar RNA host gene 8 (SNHG8) in hypoxia-ischemia-reoxygenation (HI/R)-induced myocardial injury and its potential mecha- nism of action. Cell viability, proliferation, creatine kinase myocardial band, cell apoptosis and protein expression levels were determined by Cell Counting Kit-8 assay, EdU assay, ELISA, flow cytometry and western blotting, respectively. The association between SNHG8 and microRNA (miR)-335 was confirmed using a dual-luciferase reporter gene assay. The effects of the miR-335 inhibitor transfections had on increasing apoptosis and decreasing H9C2 cell viability were reversed in cells co-transfected with SNHG8 small interfering (si)RNA. Furthermore, it was found that miR-335 could regulate RAS p21 protein activator 1 (RASA1) expression and that transfec- tion with SNHG8 siRNA downregulated RASA1 expression. Silencing of RASA1 protected against HI/R-induced H9C2 cell injury. However, SNHG8 siRNA did not further reduce apoptosis, demonstrating that SNHG8 may act through RASA1, and RASA1 may mediate the protection of SNHG8 siRNA in HI/R myocardial injury. Thus, inhibition of lncRNA SNHG8 alleviated HI/R-induced myocardial damage by regu- lating miR-335 and RASA1.