Influence of miR-127-3p on the Early Diagnosis Value and Prognostic Prediction of Ischemic Stroke in Hypertension Patients

Abstract

Background: Hypertension represents one of the most prevalent risk factors associated with ischemic stroke (IS).

Methods: A total of 102 essential hypertension (EH) patients without IS and 155 EH patients with IS were enrolled. Logistic regression analysis was performed to identify independent risk factors influencing IS. Kaplan-Meier survival analysis was used to evaluate the association between miR-127-3p expression and no recurrence in IS patients. Cox regression was applied to determine independent predictors of recurrence in IS patients. The BV-2 microglia cell line was utilized to construct an oxygen-glucose deprivation/reoxygenation (OGD/R) model, simulating ischemic injury in vitro. Flow cytometry was employed to measure cell apoptosis, while enzyme-linked immunosorbent assay was used to quantify inflammatory cytokine levels. Biochemical assay kits were applied to detect the levels of superoxide dismutase, reactive oxygen species, and malondialdehyde. Dual-luciferase reporter assays were conducted to confirm the targeting relationship.

Results: miR-127-3p was significantly upregulated in EH+IS patients and demonstrated high diagnostic value. Patients with high miR-127-3p expression exhibited a significantly increased risk of recurrence. Mechanistically, miR-127-3p played a critical role in promoting inflammation, oxidative stress, and apoptosis in OGD/R-induced neuronal injury. Akt3 was identified as a direct functional target of miR-127-3p. Suppression of miR-127-3p relieved its inhibitory effect on Akt3, thereby activating the neuroprotective function of Akt3. When Akt3 was knocked down, the protective effects mediated by the miR-127-3p inhibitor were reversed.

Conclusions: The miR-127-3p/Akt3 axis played a critical role in the regulatory mechanisms associated with EH complicated by IS.

Keywords: Akt3; hypertension; ischemic stroke; miR-127-3p; oxidative stress.