Naringenin protects myocardial ischemia/reperfusion injury by regulating miR-24-3p to inhibit cell death-inducing p53

Xiao Jin1, Ling Jin1, Bingxin Wu2

  • 1Department of Chinese Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, P. R. China.

PubMed

Insights

Naringenin, a citrus compound, protects against heart injury from ischemia/reperfusion (I/R) by increasing miR-24-3p. This microRNA helps reduce cell death by regulating Cdip1 expression, offering a potential therapeutic pathway.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Myocardial ischemia/reperfusion (I/R) injury poses significant health risks.
  • Naringenin, a citrus polyphenol, demonstrates cardioprotective properties.
  • MicroRNA-24-3p (miR-24-3p) is also recognized for its role in protecting the heart.

Purpose of the Study:

  • To investigate the potential link between naringenin's cardioprotective effects and miR-24-3p.
  • To elucidate the underlying molecular mechanisms involved in naringenin's action.

Main Methods:

  • Utilized in vivo rat myocardial I/R and in vitro H9c2 cell hypoxia/reoxygenation (H/R) models.
  • Assessed myocardial injury using histology and biochemical markers (CK, MDA, LDH).
  • Quantified miR-24-3p and Cdip1 mRNA expression via RT-PCR.

Main Results:

  • Naringenin pretreatment significantly reduced myocardial I/R injury, decreasing LDH, CK, and MDA levels.
  • Naringenin administration led to increased expression of miR-24-3p.
  • miR-24-3p was found to partially alleviate I/R injury by regulating Cdip1 expression.

Conclusions:

  • Naringenin exerts cardioprotective effects against I/R injury, partly mediated by the miR-24-3p/Cdip1 axis.
  • The findings suggest naringenin inhibits Cdip1 expression through miR-24-3p, offering a novel therapeutic strategy for myocardial I/R injury.