miR-128b Promotes Cerebral Infarction by Regulating the Expressions of BCL-2 and CAPASE3

Jin Ma1, Lei Bao1, Xiaohua Xia1

  • 1Department of Emergency Medicine, The First People's Hospital of Kunshan, Kunshan City, Jiangsu Province, China.

World Neurosurgery
|November 28, 2018
PubMed
Abstract

Insights

MicroRNA-128b (miR-128b) exacerbates stroke damage in rats by increasing brain infarction and apoptosis. Inhibiting miR-128b offers a potential therapeutic strategy for middle cerebral artery occlusion (MCAO) by reducing these effects.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Middle cerebral artery occlusion (MCAO) is a common cause of ischemic stroke.
  • MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including apoptosis.
  • The specific role of miR-128b in MCAO-induced brain injury requires further elucidation.

Purpose of the Study:

  • To investigate the impact of miR-128b on apoptosis and related protein expression in a rat MCAO model.
  • To explore the potential of modulating miR-128b for therapeutic intervention in ischemic stroke.

Main Methods:

  • Established a rat MCAO model using the thread embolism technique.
  • Administered miR-128b agomir or antagomir via stereotaxic intracerebral injection.
  • Assessed neurological deficits, cerebral infarction volume, apoptosis, and protein expression (BCL-2, Caspase-3) using established assays.

Main Results:

  • miR-128b expression was significantly upregulated in MCAO rats compared to sham controls.
  • Overexpression of miR-128b (agomir) increased cerebral infarction area and apoptosis.
  • Inhibition of miR-128b (antagomir) reduced infarction and apoptosis, accompanied by altered BCL-2 and Caspase-3 expression.

Conclusions:

  • miR-128b promotes cerebral infarction and apoptosis in MCAO rats.
  • The mechanism involves the regulation of BCL-2 and Caspase-3 protein expression.
  • Targeting miR-128b presents a promising therapeutic avenue for ischemic stroke.

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