Downregulation of lncRNA MEG3 attenuates high glucose-induced cardiomyocytes injury by inhibiting mitochondria-mediated apoptosis pathway.

Abstract

The aim of the present work was to investigate the effects and mechanisms of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) in cardiomyocytes injury and apoptosis induced by high glucose (HG) in vitro. HG-induced rats' cardiomyocytes with si-MEG3 transfection were constructed. Cell viability and lactate dehydrogenase (LDH) level were examined using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and LDH assay kits, respectively. Cardiomyocytes apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining. The expressions of Bcl-2, Bax, cleaved caspase-9 and cleaved caspase-3 proteins were determined by Western blot. The expression of lncRNA MEG3 was measured by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). Our results indicated that the expression of MEG3 was significantly upregulated in HG-treated cardiomyocytes. The downregulation of MEG3 could attenuate cardiomyocytes injury and apoptosis by decreasing the Bax/Bcl-2 ratio, cleaved caspase-9 and cleaved caspase-3 expression. The downregulation of MEG3 could attenuate cardiomyocytes injury and apoptosis induced by HG. The molecular mechanism was associated with the inhibition of the mitochondria-mediated apoptosis pathway.