Influence of miR-127-3p on the early diagnosis value and prognostic prediction of ischemic stroke in hypertension patients

医学 逻辑回归 神经保护 氧化应激 流式细胞术 细胞凋亡 内科学 冲程(发动机) 丙二醛 炎症 肿瘤科 免疫学 胃肠病学 生物 生物化学 机械工程 工程类
作者
Jinli Chen,Jing Yang,Qian Wu,Lilong Chen,Hui Wang,Junfeng Wu
出处
期刊:American Journal of Hypertension [Oxford University Press]
标识
DOI:10.1093/ajh/hpaf201
摘要

Abstract BACKGROUND Hypertension represents one of the most prevalent risk factors associated with ischemic stroke (IS). METHODS 102 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 OGD/R model, simulating ischemic injury in vitro. Flow cytometry was employed to measure cell apoptosis, while enzyme-linked immunosorbent assay (ELISA) was used to quantify inflammatory cytokine levels. Biochemical assay kits were applied to detect the levels of superoxide dismutase (SOD), reactive oxygen species (ROS), and malondialdehyde (MDA). 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.
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