Conclusion
GABPB1-AS1 silencing alleviated CI/R injury through the miR-641/NUCKS1 axis, indicating that GABPB1-AS1 might serve as a therapeutic target for CI/R injury.
Methods
RT-qPCR was applied to determine GABPB1-AS1 expression in oxygen-glucose deprivation/reoxygenation (OGD/R) cells. The targeting relationships between GABPB1-AS1 and miR-641, as well as between miR-641 and nuclear casein and cyclin-dependent kinase substrate 1 (NUCKS1) were examined by dual luciferase reporter assay. The protein expression of caspase-3, Bax, Bcl-2 and NUCKS1 was examined by western blot. Cell apoptosis was measured by flow cytometry (FCM) and western blot. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
Objective
To investigate the possible mechanism of lncRNA GA binding protein transcription factor beta subunit 1 antisense RNA 1 (GABPB1-AS1) in cerebral ischemia/reperfusion (CI/R) injury.
Results
GABPB1-AS1 was significantly elevated in SH-SY5Y cells under OGD/R. Downregulation of GABPB1-AS1 accelerated cell viability and suppressed cell apoptosis. GABPB1-AS1 silencing reduced ROS and MDA levels in OGD/R-treated cells. Furthermore, miR-641 inhibitor aggravated damage from OGD/R, but GABPB1-AS1 silencing notably attenuated this effect. NUCKS1 was proven to be a target gene of miR-641.