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Neuroprotective Influence of miR-301a Inhibition in Experimental Cerebral Ischemia/Reperfusion Rat Models Through

Tao Feng1, Bang-Hua Han1, Gong-Li Yang1

  • 1Department of Neurosurgery, Shanxian Central Hospital, Shanxian, 274300, Shandong, China.

Journal of Molecular Neuroscience : MN
|March 22, 2019
PubMed

Insights

Inhibiting microRNA-301a (miR-301a) shows neuroprotective effects in cerebral ischemia-reperfusion injury by reducing cell apoptosis and inflammation. This occurs possibly by targeting NDRG2, suggesting a new therapeutic avenue.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Cerebral ischemia-reperfusion (I/R) injury is a critical condition with significant neurological consequences.
  • MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including those involved in I/R injury.
  • The specific role of miR-301a in cerebral I/R injury and its potential molecular targets require further elucidation.

Purpose of the Study:

  • To investigate the influence of miR-301a on experimental cerebral ischemia-reperfusion (I/R) injury in a rat model.
  • To explore the potential targeting relationship between miR-301a and NDRG2 in the context of cerebral I/R injury.
  • To evaluate the therapeutic potential of modulating miR-301a levels for mitigating I/R-induced damage.

Main Methods:

  • Establishment of a rat model for cerebral I/R injury with various experimental groups (model, sham, miR-301a inhibitor, miR-301a mimic, siNDRG2, NDRG2, and combined treatments).
  • Assessment of cerebral infarct volume and cell apoptosis using TTC and TUNEL staining, respectively.
  • Verification of the miR-301a and NDRG2 interaction using dual-luciferase reporter gene assay; quantification of molecular expressions via ELISA, qRT-PCR, and Western blot.

Main Results:

  • Rats with cerebral I/R injury exhibited increased neurological deficit, infarct volume, cell apoptosis, and inflammatory response, accompanied by elevated miR-301a and NDRG2 expression compared to the sham group.
  • Administration of miR-301a inhibitor or NDRG2 reversed these detrimental effects, while miR-301a mimic or siNDRG2 exacerbated them.
  • Dual-luciferase assay confirmed NDRG2 as a direct target of miR-301a, and knockdown of NDRG2 counteracted the protective effects of the miR-301a inhibitor.

Conclusions:

  • Inhibiting miR-301a demonstrates a significant neuroprotective effect in cerebral I/R injury rats.
  • This protective mechanism involves the amelioration of cell apoptosis and inflammatory response, likely through the downregulation of its target gene, NDRG2.
  • Modulating miR-301a-NDRG2 interaction presents a potential therapeutic strategy for treating cerebral ischemia-reperfusion injury.
Keywords:
ApoptosisCerebral ischemia-reperfusion injuryNDRG2miR-301a

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