Related Experiment Video
Updated: Jul 16, 2025
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
miR-26a Improves Microglial Activation and Neuronal Apoptosis in a Rat Model of Cerebral Infarction by Regulating the
1Department of Neurology, Bazhong Central Hospital, Bazhong, China.
Abstract:
Emerging studies have indicated that abnormally expressed microRNAs (miRNAs) are related to the pathogenesis of cerebral ischemia. Nevertheless, the function of miR-26a in neuronal damage and microglial activation during cerebral infarction remains elusive. It was revealed that miR-26a was downregulated in oxygen-glucose deprivation (OGD)-treated microglia and neurons. Overexpressing miR-26a reduced the inflammatory reaction in BV2 cells and decreased neuronal apoptosis following OGD stimulation. miR-26a upregulation inactivated the TLR4/MyD88/NF-κB pathway and inhibited TREM1 expression. Repressing NF-κB phosphorylation inhibited the miR-26a level. As supported by the dual-luciferase reporter assay, TREM1 was directly targeted by miR-26a. Furthermore, a rat model of middle cerebral artery occlusion (MCAO) was built. We discovered that miR-26a improved cognitive, learning, and motor functions and reduced cerebral edema in MCAO rats. Mechanistically, upregulating miR-26a reduced inflammation and neuronal apoptosis by mitigating the TREM1-TLR4/MyD88/NF-κB pathway in the MCAO rat model. Collectively, this study verified that the miR-26a-TREM1-TLR4/MyD88/NF-κB axis contributes to modulating OGD-mediated microglial activation and neuronal injury.
Insights
MicroRNA-26a (miR-26a) protects against brain damage after stroke by reducing inflammation and neuronal death. Upregulating miR-26a inhibits the TREM1-TLR4/MyD88/NF-κB pathway, improving outcomes in cerebral infarction models.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are implicated in cerebral ischemia pathogenesis.
- The specific role of miR-26a in neuronal injury and microglial activation during cerebral infarction is not fully understood.
Purpose of the Study:
- To investigate the function and mechanism of miR-26a in neuronal damage and microglial activation in cerebral infarction.
Main Methods:
- Oxygen-glucose deprivation (OGD) model in microglia and neurons.
- Overexpression of miR-26a.
- Middle cerebral artery occlusion (MCAO) rat model.
- Dual-luciferase reporter assay.
- Analysis of the TLR4/MyD88/NF-κB pathway and TREM1 expression.
Main Results:
- miR-26a was downregulated in OGD-treated cells.
- Overexpressing miR-26a reduced inflammation and neuronal apoptosis in vitro.
- miR-26a inactivated the TLR4/MyD88/NF-κB pathway and inhibited TREM1.
- TREM1 was identified as a direct target of miR-26a.
- In MCAO rats, miR-26a improved cognitive, learning, and motor functions and reduced cerebral edema.
- miR-26a mitigated the TREM1-TLR4/MyD88/NF-κB pathway, reducing inflammation and neuronal apoptosis.
Conclusions:
- The miR-26a-TREM1-TLR4/MyD88/NF-κB axis plays a crucial role in modulating microglial activation and neuronal injury during cerebral infarction.
- miR-26a demonstrates therapeutic potential for treating cerebral ischemia.
