ArticleHereditas2025
Silencing LncRNA HCG27 ameliorates cognitive dysfunction after ischemic stroke via miR-27a-3p regulation.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Molecular Mechanism of LncRNA LUCAT1 Regulating HSPB8 Expression via miR-337-3p in Modulating Neurological Damage After Cerebral Infarction.Neurochemical research · 2026Article
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- IncRNAs transcriptomics elucidates the potential mechanism of Naoshuantong capsule in alleviating synaptic dysfunction in a murine model of cerebral ischemia/reperfusion injury.Frontiers in pharmacology · 2026Article
- 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.Neurochemical research · 2025Article
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Authors and funding
8 authors.
Funding
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Abstract
backgroundWe explore the effect of improving cognitive dysfunction after cerebral ischemia-reperfusion (CI/R) by regulating HCG27.
methodsThe MCAO and OGD/R methods were employed to establish in vivo and in vitro models of cognitive dysfunction caused by a CI/R injury. RT-qPCR was utilized to detect the relative expression of HCG27 and miR-27a-3p. An ELISA was adopted to measure the concentrations of inflammatory factors (IL-6, IL-1β, IL-10). The concentration of MDA and activity of CAT were detected using commercially available kits. The neurological deficit was evaluated using the mNSS score. The spatial learning and memory capabilities were evaluated via the MWM test. The targeting relationships were validated by the dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. The CCK-8 assay and flow cytometry were employed to asses cell viability and apoptosis, respectively.
resultsThe level of HCG27 was upregulated in MCAO rats and OGD/R-induced BV2 cells, whereas that of miR-27a-3p decreased, and HCG27 targeted miR-27a-3p. Compared with the sham group, the mNSS score of MCAO rats was elevated, and their spatial learning and memory abilities declined, with aggravated inflammatory response and oxidative stress. However, silencing HCG27 improved these conditions, and the miR-27a-3p antagonist reversed this. MiR-27a-3p reversed the increase in cell viability in OGD/R-induced BV2 cells, reduced the cell apoptosis rate, and weakened the inflammatory response and oxidative stress caused by the HCG27 silencing.
conclusionsSilencing HCG27 can protect against cognitive dysfunction after cerebrovascular disease by targeting miR-27a-3p.
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