MicroRNA-532-5p upregulation protects neurological deficits after ischemic stroke through inhibition of BTB and CNC homology 1

Abstract Objective MicroRNA (miR)-532-5p has been reported to protect against ischemic stroke (IS), while the underlying mechanism of miR-532-5p targeting BTB and CNC homology 1 (BACH1) in IS remains unknown. Thus, we aim to detect the role of miR-532-5p in IS via targeting BACH1. Methods Blood samples were collected from IS patients and healthy controls. Rat middle cerebral artery occlusion (MCAO) models were established and intracerebrally injected with altered miR-532-5p or BACH1 plasmid vectors to reveal their roles in neurological function, brain tissue pathology and inflammation in MCAO. Expression of miR-532-5p and BACH1 in patients’ blood samples and rat brain tissues was assessed, and the targeting relationship between miR-532-5p and BACH1 was confirmed. Results MiR-532-5p was downregulated and BACH1 was upregulated in IS. BACH1 was targeted by miR-532-5p. Restored miR-532-5p or inhibited BACH1 improved neurological function and inhibited inflammation and apoptosis in MCAO rats. On the contrary, miR-532-5p reduction or BACH1 overexpression had totally opposite effects on MCAO rats. The protective role of miR-532-5p for MCAO rats was reversed by upregulated BACH1. Conclusion MiR-532-5p upregulation protects against neurological deficits after IS through inhibition of BACH1.