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Updated: Jan 26, 2026

Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.
Xi Zhang1,2, Xiao-Lei Zhu1,2, Bi-Ying Ji1,2
1Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, 210008, China.
LncRNA-1810034E14Rik is decreased in ischemic stroke models. Overexpressing this long non-coding RNA reduces brain damage and inflammation, suggesting it as a therapeutic target.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Microglial cell activation is crucial in neuroinflammation following ischemic stroke.
- Inhibiting microglial activation presents a potential therapeutic strategy for stroke treatment.
Purpose of the Study:
- To investigate the role of long non-coding RNAs (lncRNAs) in microglial cell inflammation during ischemic stroke.
- To determine the therapeutic potential of LncRNA-1810034E14Rik in ischemic stroke models.
Main Methods:
- Established in vitro (oxygen-glucose deprivation) and in vivo (MCAO mouse model) ischemic stroke models.
- Utilized microarray, RT-qPCR, ELISA, immunofluorescence, and Western blotting to analyze lncRNA and inflammatory marker expression and microglial activation.
Main Results:
- LncRNA-1810034E14Rik expression was significantly reduced in ischemic conditions.
- Overexpression of LncRNA-1810034E14Rik decreased infarct volume and brain damage in MCAO mice.
- LncRNA-1810034E14Rik suppressed microglial activation, inflammatory cytokine production, and p65 phosphorylation.
Conclusions:
- LncRNA-1810034E14Rik exhibits an anti-inflammatory role in ischemic stroke.
- This lncRNA regulates p65 phosphorylation, indicating its potential as a therapeutic target for stroke treatment.
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