A preliminary study on miR-1271-5p as a potential biomarker of post-stroke cognitive impairment and its exacerbation of neuroinflammation and oxidative stress by targeting IGFBP3

Stroke is a leading cause of long-term functional and cognitive impairment. Post-stroke cognitive impairment (PSCI) lacks sensitive and specific diagnostic methods. MicroRNAs (miRNAs), particularly miR-1271-5p, have emerged as potential biomarkers in neurological disorders, but their role in PSCI remains unclear. The objective of this study was to evaluate the diagnostic and predictive value of miR-1271-5p in PSCI and to explore its molecular mechanism through the IGFBP3 pathway in microglial cells. A total of 102 stroke patients (54 with PSCI, 48 without) and 60 healthy controls were enrolled. miR-1271-5p expression was measured by qRT-PCR. Diagnostic and predictive performance was evaluated using ROC curves and logistic regression. In vitro, HMC3 microglial cells were exposed to oxygen–glucose deprivation/reperfusion (OGD/R) to model ischemic injury. Dual-luciferase assay, CCK-8, ELISA, and rescue experiments were performed to verify the miR-1271-5p/IGFBP3 axis. miR-1271-5p was markedly upregulated in stroke and PSCI patients (P < 0.001), showing strong diagnostic accuracy (AUC = 0.879). High miR-1271-5p expression was independently associated with PSCI (OR = 7.434, 95% CI = 2.658–20.793, P < 0.001) and correlated with disease severity. IGFBP3 was characterized as a downstream target of miR-1271-5p. In OGD/R-treated microglia, miR-1271-5p inhibition alleviated inflammation and oxidative stress, effects reversed by IGFBP3 knockdown. miR-1271-5p is a promising predictive biomarker for PSCI and exacerbates neuroinflammation and oxidative stress by targeting IGFBP3, highlighting its potential as a therapeutic target.