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Abstract <p>Long non-coding RNAs (lncRNAs) showed essential regulated function in mediating neuroinflammatory responses following ischemic stroke (IS). This study aims to elucidate the function and mechanism of lncRNA PRR34-AS1 in neuroinflammatory responses during IS. Serum levels of PRR34-AS1 were measured by quantitative real-time PCR (RT-qPCR) in 80 IS patients and 80 healthy controls. The oxygen-glucose deprivation/reperfusion (OGD/R) model of human microglial HMC3 cells was conducted to simulate ischemic conditions. The diagnosis of PRR34-AS1 in IS was evaluated using the ROC curve. The Pearson correlation coefficient was used to assess the relationship between PRR34-AS1 and NHISS scores. And the HMC3 cell inflammatory cytokine levels (TNF-α, IL-6, IL-1β), and miR-532-3p expression were measured by ELISA and RT-qPCR. PRR34-AS1 was upregulated in IS patients and OGD/R-induced HMC3 cells. Conversely, miR-532-3p levels were decreased in OGD/R-induced HMC3 cells. Additionally, both suppressing PRR34-AS1 and overexpressing miR-532-3p protected OGD/R-induced HMC3 cells from inflammation damage. Moreover, miR-532-3p was negatively regulated by PRR34-AS1, and its overexpression effectively reversed the inflammatory effects caused by PRR34-AS1 overexpression. PRR34-AS1 promoted neuroinflammation during IS by regulating miR-532-3p. Targeting this axis may present novel therapeutic strategies to mitigate neuronal damage following IS.</p>

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LncRNA PRR34-AS1 Promoted the Neuroinflammation of Ischemic Stroke via Regulating miR-532-3p

  • 期刊论文

  • 发表日期：

    2026年7月19日

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  • Huiting Zhang,
  • Kuilong Zhou,
  • Zhijie Liang,
  • Yangjie Song,
  • Xiaomin Yang

摘要

Abstract

Long non-coding RNAs (lncRNAs) showed essential regulated function in mediating neuroinflammatory responses following ischemic stroke (IS). This study aims to elucidate the function and mechanism of lncRNA PRR34-AS1 in neuroinflammatory responses during IS. Serum levels of PRR34-AS1 were measured by quantitative real-time PCR (RT-qPCR) in 80 IS patients and 80 healthy controls. The oxygen-glucose deprivation/reperfusion (OGD/R) model of human microglial HMC3 cells was conducted to simulate ischemic conditions. The diagnosis of PRR34-AS1 in IS was evaluated using the ROC curve. The Pearson correlation coefficient was used to assess the relationship between PRR34-AS1 and NHISS scores. And the HMC3 cell inflammatory cytokine levels (TNF-α, IL-6, IL-1β), and miR-532-3p expression were measured by ELISA and RT-qPCR. PRR34-AS1 was upregulated in IS patients and OGD/R-induced HMC3 cells. Conversely, miR-532-3p levels were decreased in OGD/R-induced HMC3 cells. Additionally, both suppressing PRR34-AS1 and overexpressing miR-532-3p protected OGD/R-induced HMC3 cells from inflammation damage. Moreover, miR-532-3p was negatively regulated by PRR34-AS1, and its overexpression effectively reversed the inflammatory effects caused by PRR34-AS1 overexpression. PRR34-AS1 promoted neuroinflammation during IS by regulating miR-532-3p. Targeting this axis may present novel therapeutic strategies to mitigate neuronal damage following IS.