Objective: Diabetic cardiomyopathy (DCM) is an important complication of diabetes. This study was attempted
to discover the effects of long noncoding RNA OIP5-AS1 (OIP5-AS1) on the viability and oxidative stress of cardiomyocyte
in DCM.
Methods: The expression of OIP5-AS1 and microRNA-34a (miR-34a) in DCM was detected by qRT-PCR. In vitro, DCM
was simulated by high glucose (HG, 30 mM) treatment in H9c2 cells. The viability of HG (30 mM)-treated H9c2 cells was
examined by MTT assay. The reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA)
levels were used to evaluate the oxidative stress of HG (30 mM)-treated H9c2 cells. Dual-luciferase reporter assay was used
to confirm the interactions among OIP5-AS1, miR-34a and SIRT1. Western blot was applied to analyze the protein expression
of SIRT1.
Results: The expression of OIP5-AS1 was down-regulated in DCM, but miR-34a was up-regulated. The functional experiment
stated that OIP5-AS1 overexpression increased the viability and SOD level, while decreased the ROS and MDA levels
in HG (30 mM)-treated H9c2 cells. The mechanical experiment confirmed that OIP5-AS1 and SIRT1 were both targeted by
miR-34a with the complementary binding sites at 3′UTR. MiR-34a overexpression inhibited the protein expression of
SIRT1. In the feedback experiments, miR-34a overexpression or SIRT1 inhibition weakened the promoting effect on viability,
and mitigated the reduction effect on oxidative stress caused by OIP5-AS1 overexpression in HG (30 mM)-treated H9c2
cells.
Conclusions: OIP5-AS1 overexpression enhanced viability and attenuated oxidative stress of cardiomyocyte via regulating
miR-34a/SIRT1 axis in DCM, providing a new therapeutic target for DCM.
Long Noncoding RNA OIP5-AS1 Inhibits Cell Apoptosis and Cataract Formation by Blocking POLG Expression Under Oxidative Stress