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Nicorandil reversed homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway

Biming Zhan1, Zongyu Xu2, Yang Zhang3

  • 1Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|May 15, 2020
PubMed

Insights

Nicorandil protects against coronary microvascular dysfunction in hyperhomocysteinemia (HHcy) and acute myocardial infarction (AMI). It works by activating the PI3K/Akt/eNOS pathway, improving cardiac function and microcirculation.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Cell Biology

Background:

  • Coronary microvascular dysfunction is a key issue in acute myocardial infarction (AMI).
  • Hyperhomocysteinemia (HHcy) exacerbates AMI, but nicorandil's role in HHcy-related AMI is unclear.
  • Understanding nicorandil's mechanism in HHcy-AMI is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the protective mechanism of nicorandil in hyperhomocysteinemia-induced coronary microvascular dysfunction in acute myocardial infarction.
  • To elucidate the role of the PI3K/Akt/eNOS signaling pathway in nicorandil's effects.

Main Methods:

  • Established in vitro (human coronary artery endothelial cells) and in vivo (C57/BL6 mice) models of HHcy and AMI.
  • Assessed cardiac function using small animal ultrasound.
  • Evaluated microcirculation via CD31 and tomato lectin staining.
  • Determined cellular effects and pathway activation using MTT, tube formation, and Western blotting assays.

Main Results:

  • Nicorandil enhanced endothelial cell viability and promoted the PI3K/Akt/eNOS pathway in vitro.
  • In vivo, nicorandil improved cardiac function (LVEF, LVFS) and microcirculation markers (CD31, tomato lectin).
  • Inhibition of PI3K or NOS pathways abolished nicorandil's beneficial effects.

Conclusions:

  • Nicorandil demonstrates a protective effect against HHcy-induced coronary microvascular dysfunction in AMI.
  • The PI3K/Akt/eNOS signaling pathway mediates the beneficial actions of nicorandil.
  • Findings support nicorandil as a potential therapeutic agent for HHcy-AMI patients.
Abstract

Keywords:
Coronary microvascular dysfunctionHomocysteineNicorandilPI3K/Akt/eNOS pathway

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