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.

Bioengineered
|June 11, 2021
PubMed

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.