LncRNA MCM3AP-AS1 protects against cerebral ischemia-reperfusion injury via targeting miR-27b-3p

Cerebral ischemia-reperfusion (CI/R) injury is a significant hurdle in ischemic stroke treatment. Substantial evidence indicates that long non-coding RNAs (lncRNAs) are implicated in CI/R injury. Here, we explore the function of lncRNA MCM3AP-AS1 in CI/R injury. Employed the middle cerebral artery occlusion/reperfusion (MCAO/R) mice model and oxygen-glucose deprivation/reoxygenation (OGD/R) HT22 cell model to mimic in vivo and in vitro CI/R injury. Morris water maze test assessed mice platform-finding latency and swimming distance. Real-time quantitative reverse transcription PCR were conducted to examine the levels of MCM3AP-AS1 and microRNA (miR)-27b-3p. Modified Neurological Severity Score (mNSS) assessed neurological deficits, and triphenyl tetrazolium chloride staining assessed cerebral infarct volume. Enzyme-linked immunosorbent assay quantified inflammatory factor levels. Cell count kit-8 and flow cytometry detected cell viability and apoptosis, respectively. Dual luciferase reporter and RNA immunoprecipitation assays verified targeting relationships. MAMC3AP-AS1 expression decreased in the brain tissue of MCAO/R mice and OGD/R-treated cells, while miR-27b-3p levels were rose. Upregulating MCM3AP-AS1 notably suppressed mNSS scores, reduced infarct volume, and alleviated cognitive dysfunction in MCAO/R mice; however, miR-27b-3p attenuated the function of MCM3AP-AS1. Furthermore, OGD/R treatment inhibited cell viability, increased apoptosis, and promoted inflammatory factors secretion, MCM3AP-AS1 reversed these effects, but miR-27b-3p significantly impaired this reversal. Mechanistically, MCM3AP-AS1 targeted miR-27b-3p. MCM3AP-AS1 exerts neuroprotection by attenuating miR-27b-3p levels, thereby mitigating CI/R injury.