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
摘要
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.
MethodsA 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.
ResultsmiR-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.
ConclusionsmiR-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.