ArticleNeurochemical research2025
NEXN-AS1 Predicts the Occurrence of Post-Stroke Cognitive Impairment and Alleviates Inflammation and Oxidative Stress by Targeting the miR-92a-3p/NRF1 Axis : NEXN-AS1 Alleviates Inflammation and Oxidative Stress in PSCI.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- LncRNA HOTAIR/miR-9-5p/FOXP1 axis modulates cerebral ischemia-reperfusion injury via NLRP3 inflammasome activation.IBRO neuroscience reports · 2026Article
- Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026Review
- Integrative Analysis of Trace Elements, Oxidative Stress, and Psychological Distress in Epilepsy: Biochemical Profiling and In Silico Docking Insights.Neurochemical research · 2026Article
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7 authors.
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Abstract
Post-stroke cognitive impairment (PSCI) is a prevalent cerebrovascular condition resulting from ischemic stroke. This study aimed to determine the expression levels of NEXN-AS1 in PSCI, evaluate its clinical significance, and further uncover the molecular mechanisms through which it contributes to the initiation and progression of PSCI. The quantification of NEXN-AS1, miR-92a-3p, and NRF1 expression was performed using qRT-PCR. The diagnostic utility of serum NEXN-AS1 was assessed through ROC analysis. Risk factors associated with cognitive impairment following stroke were identified using both univariate and multivariate logistic regression. A cellular model of cognitive dysfunction was established via oxygen-glucose deprivation/reperfusion (OGD/R). The PSCI animal model was established through the Middle cerebral artery occlusion (MCAO) surgery. Inflammatory status was determined by measuring cytokine levels, including IL-6, IL-1β, and IL-10, while oxidative stress was evaluated by quantifying ROS, MDA, and CAT. In stroke patients, NEXN-AS1 expression was notably downregulated and further decreased in cases with PSCI. It served as a reliable biomarker for distinguishing stroke patients from healthy individuals and PSCI from post-stroke cognitive normality (PSCN) groups. Upregulation of NEXN-AS1 in BV2 cells following OGD/R stimulation led to increased proliferation, decreased inflammatory response, and reduced oxidative stress. Moreover, miR-92a-3p expression reversed the protective effects of NEXN-AS1 under OGD/R conditions. Overexpression of NEXN-AS1 alleviated cognitive dysfunction, inflammatory response and oxidative stress in PSCI rats, while overexpression of miR-92a-3p counteracted the protective effect of NEXN-AS1 on PSCI rats. Further analysis identified NRF1 as a downstream target of miR-92a-3p. NEXN-AS1 exerts protective effect against ischemic brain injury in both in vitro and in vivo models by regulating miR-92a-3p. Therefore, NEXN-AS1 may predict the occurrence of PSCI, and NEXN-AS1 may contribute to PSCI pathogenesis via regulation of the miR-92a-3p/NRF1 axis.
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