AIM To investigate the effect of long non coding RNA (lnc RNA) maternally expressed gene 3 (MEG3) on hypoxia/reoxygenation (H/R) induced myocardial cell injury by regulating the miR-138-5p/high mobility group protein A1 (HMGA1) axis.

METHODS H9c2 cells cultured in vitro were randomly separated into: NC group (normal H9c2 cells), H/R, si-NC group, si-MEG3 group, mimic NC group, miR-138-5p mimic group, si-MEG3+inhibitor NC group, and si-MEG3+miR-138-5p inhibitor group. Except for the NC group, the remaining 7 groups were transfected with corresponding substances to construct an H/R model. qRT-PCR method was applied to determine the mRNA expression levels of MEG3, miR-138-5p, and HMGA1 in each group. CCK-8 method and flow cytometry assay were performed to measure the cellproliferation and apoptosis in each group. ELISA method was applied to determine the levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), and malondialdehyde (MDA). Western blot was applied to detect the expression of Bax and Bcl-2. Dual luciferase reporter gene experiment was applied to detect the targeting relationship between MEG3 and miR-138-5p, and between HMGA1 and miR-138-5p.

RESULTS Compared with the NC group, the OD450 value, SOD, and Bcl-2 protein expression in the H/R group decreased, while the apoptosis rate, MDA, LDH, and Bax protein expression increased (P<0.05). Silence of MEG3 or overexpression of miR-138-5p was able to antagonize the above changes (P<0.05). Inhibiting the expression of miR-138-5p on the basis of silencing MEG3 can decrease the expression of miR-138-5p in H/ R-induced H9c2 cells, inhibit cell proliferation, and promote HMGA1 expression, apoptosis and oxidative stress (P<0.05). The dual luciferase reporter gene experiment confirmed that miR-138-5p had a targeted regulatory relationship with MEG3 and HMGA1 (P<0.05).

CONCLUSION Silencing MEG3 promotes H/R induced proliferation of H9c2 cells, inhibits their oxidative stress and apoptosis, which may be related to the regulation of miR-138-5p/HMGA1 axis.