Related Experiment Video
Updated: Nov 2, 2025

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
MicroRNA miR-126 attenuates brain injury in septic rats via NF-κB signaling pathway
Anna Nong1, Qingfeng Li2, Zhijing Huang3
1Graduate School, Youjiang Medical University for Nationalities, Baise, Guangxi China.
Abstract:
The purpose of this study was to investigate the impact and mechanism of microRNA miR-126 on brain injury induced by blood-brain barrier (BBB) damage in septic rats. We used cecal ligation and perforation (CLP) to create a rat model of sepsis. The experimental rats were randomly divided into Control group, CLP group, CLP + miR-NC group, CLP + miR-126 group and CLP + miR-126 + NF-κB pathway agonist (PMA) group. MiR-126 expressed in the brain tissue of CLP rats was down-regulated by qRT-PCR. Upregulation of miR-126 in CLP rats could improve brain injury and BBB marker protein level, reduce brain water content, Evans blue extravasation, inflammation, and excessive oxidative stress. This could also result in an inhibition of NF-κB signaling pathway activity. In conclusion, miR-126 overexpression can prevent brain injury caused by BBB damage via the inhibition of NF-κB signaling pathway activity.
Insights
MicroRNA miR-126 protects against sepsis-induced brain injury by strengthening the blood-brain barrier (BBB). Upregulating miR-126 reduces inflammation and oxidative stress by inhibiting the NF-κB pathway.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Sepsis can lead to brain injury due to blood-brain barrier (BBB) damage.
- MicroRNAs (miRNAs) play a role in regulating cellular processes, including those involved in brain injury.
Purpose of the Study:
- To investigate the role and mechanism of microRNA miR-126 in sepsis-induced brain injury associated with BBB damage.
- To determine if miR-126 can mitigate brain injury in a rat model of sepsis.
Main Methods:
- A rat model of sepsis was established using cecal ligation and perforation (CLP).
- Quantitative real-time PCR (qRT-PCR) was used to measure miR-126 expression in brain tissue.
- Rats were divided into control, CLP, and treatment groups, including those receiving miR-126 mimics or inhibitors.
- Brain injury markers, water content, Evans blue extravasation, inflammation, oxidative stress, and NF-κB pathway activity were assessed.
Main Results:
- Sepsis induction (CLP) led to down-regulation of miR-126 in brain tissue.
- Overexpression of miR-126 in CLP rats improved brain injury and BBB integrity.
- miR-126 upregulation reduced brain water content, Evans blue extravasation, inflammation, and oxidative stress.
- Inhibition of the NF-κB signaling pathway was observed with miR-126 overexpression.
Conclusions:
- miR-126 plays a protective role in sepsis-induced brain injury.
- Overexpression of miR-126 mitigates brain injury by preserving BBB function and reducing neuroinflammation.
- The protective effects of miR-126 are mediated through the inhibition of the NF-κB signaling pathway.

