Volume 46 Issue 10
Oct.  2025
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Zhiyong LI, Zhenggang CHEN, Jun PENG, Dazhong LIANG. miR-16-5p Promotes Inflammation and Apoptosis in Oxygen-Glucose Deprivation Microglia Model by Mediating GPR30 Expression[J]. Journal of Kunming Medical University, 2025, 46(10): 23-31. doi: 10.12259/j.issn.2095-610X.S20251003
Citation: Zhiyong LI, Zhenggang CHEN, Jun PENG, Dazhong LIANG. miR-16-5p Promotes Inflammation and Apoptosis in Oxygen-Glucose Deprivation Microglia Model by Mediating GPR30 Expression[J]. Journal of Kunming Medical University, 2025, 46(10): 23-31. doi: 10.12259/j.issn.2095-610X.S20251003

miR-16-5p Promotes Inflammation and Apoptosis in Oxygen-Glucose Deprivation Microglia Model by Mediating GPR30 Expression

doi: 10.12259/j.issn.2095-610X.S20251003
  • Received Date: 2025-06-25
    Available Online: 2025-09-25
  • Publish Date: 2025-10-28
  •   Objective  To explore the molecular mechanism of miR-16-5p promoting apoptosis and inflammatory response by targeting GPR30 expression in an in vitro ischemic stroke microglia model (BV-2).  Methods  An ischemic stroke cell model was established by subjecting BV-2 cells to oxygen-glucose deprivation (OGD). qRT-PCR was utilized to assess the levels of miR-16-5p and GPR30 mRNA in OGD cells. A miR-16-5p inhibitor was transfected into OGD cells to silence miR-16-5p expression, and alterations in inflammatory response and apoptosis were measured using ELISA kits and Annexin V-FITC/PI staining. Starbase was employed to predict interactions, and dual-luciferase reporter gene assays were conducted to confirm that miR-16-5p targets the 3'-untranslated region (UTR) sequence of GPR30. Changes in cellular inflammatory response and apoptosis were evaluated by knocking down miR-16-5p and/or GPR30 in OGD cells.  Results  miR-16-5p expression was significantly elevated (P < 0.01), while GPR30 expression was notably decreased (P < 0.01) in OGD-induced cells. Knockdown of miR-16-5p reduced the expression levels of inflammatory factors and the cell apoptosis ratio (P < 0.01). Inhibition of miR-16-5p expression led to an upregulation of GPR30 mRNA and protein levels (P < 0.01). Simultaneous silencing of both miR-16-5p and GPR30 partially enhanced inflammatory factor expression levels and the cell apoptosis ratio compared to cells transfected solely with the miR-16-5p inhibitor (P < 0.05).   Conclusion  In the microglia OGD model, miR-16-5p triggers inflammatory responses and enhances apoptosis by inhibiting GPR30 expression.
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