Related Experiment Video
Updated: Nov 8, 2025
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
miR-671-5p Attenuates Neuroinflammation via Suppressing NF-κB Expression in an Acute Ischemic Stroke Model
Ling Deng1,2, Yi Guo3, Jingdong Liu1
1College of Pharmacology, The Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Abstract:
This study was designed to investigate the role of miR-671-5p in in vitro and in vivo models of ischemic stroke (IS). Middle cerebral artery occlusion and reperfusion (MCAO/R) in C57BL/6 mice as well as oxygen-glucose deprivation and reoxygenation (OGD/R) in a mouse hippocampal HT22 neuron line were used as in vivo and in vitro models of IS injury, respectively. miR-671-5p agomir, miR-671-5p antagomir, pcDNA3.1-NF-κB, and negative controls were transfected into cells using riboFECT CP reagent. miR-671-5p agomir, pcDNA3.1-NF-κB, and negative vectors were administered into MCAO/R mice via intracerebroventricular injection. The results showed that miR-671-5p was significantly downregulated and that miR-671-5p agomir alleviated injury and neuroinflammation induced by ischemic reperfusion. A dual-luciferase reporter assay confirmed that NF-κB is a direct target of miR-671-5p. Reverse experiments showed that miR-671-5p agomir reduced neuroinflammation via suppression of NF-κB expression in both in vitro and in vivo models of IS. Our data suggest that miR-671-5p may be a viable therapeutic target for diminishing neuroinflammation in patients with IS.
Insights
MicroRNA-671-5p (miR-671-5p) is downregulated in ischemic stroke (IS). Restoring miR-671-5p levels reduces brain injury and neuroinflammation by targeting NF-κB.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Ischemic stroke (IS) is a leading cause of death and disability.
- Neuroinflammation plays a critical role in IS pathogenesis.
- MicroRNAs (miRNAs) are implicated in regulating IS.
Purpose of the Study:
- To investigate the role of miR-671-5p in ischemic stroke (IS).
- To explore miR-671-5p as a potential therapeutic target for IS.
Main Methods:
- Established in vivo (MCAO/R) and in vitro (OGD/R) models of IS.
- Utilized miR-671-5p agomir and antagomir for modulation.
- Confirmed NF-κB as a direct target of miR-671-5p using dual-luciferase reporter assay.
Main Results:
- miR-671-5p expression was significantly downregulated in IS models.
- miR-671-5p agomir administration alleviated IS-induced injury and neuroinflammation.
- miR-671-5p reduced neuroinflammation by suppressing NF-κB expression.
Conclusions:
- miR-671-5p plays a protective role in IS.
- Targeting miR-671-5p may offer a novel therapeutic strategy for IS.
- Suppression of NF-κB by miR-671-5p is a key mechanism in mitigating IS neuroinflammation.
