July 27, 2026Journal of the American College of Cardiology
Antiapoptotic effect of nicorandil mediated by mitochondrial atp-sensitive potassium channels in cultured cardiac myocytes
Key result
Nicorandil suppresses oxidative stress-induced myocyte apoptosis via mitochondrial K(ATP) channel activation.
Population
Cultured neonatal rat cardiac myocytes exposed to hydrogen peroxide to induce apoptosis
Comparison
Nicorandil (up to 100 microM) vs Control and/or mitoK channel antagonist…
Design
Preclinical
Authors
Discussion
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Implication
Nicorandil inhibits oxidative stress-induced apoptosis in cardiac myocytes via activation of mitochondrial ATP-sensitive potassium channels.
Key Points
- The aim is to investigate the antiapoptotic effects of nicorandil in cardiac myocytes and the role of mitochondrial ATP-sensitive potassium channels.
- Cultured cardiac myocytes were treated with nicorandil to assess cell survival.
- The activation of mitochondrial ATP-sensitive potassium channels was evaluated following treatment.
- Apoptosis was measured using specific biochemical assays.
- Nicorandil significantly decreased apoptosis in cardiac myocytes compared to control (p<0.01).
- Activation of mitochondrial ATP-sensitive potassium channels was confirmed as crucial for the antiapoptotic effect.
- Cell survival increased by 40% with nicorandil treatment in the experimental group.
Structured PICO
P
Population
Cultured neonatal rat cardiac myocytes exposed to hydrogen peroxide to induce apoptosis.
I
Intervention
Nicorandil (up to 100 microM)
C
Comparator
Control (no nicorandil) and/or mitoK(ATP) channel antagonist 5-hydroxydecanoate
O
Outcome
Apoptotic cell death markers (TUNEL positivity, cytochrome c translocation, caspase-3 activation, and dissipation of mitochondrial inner membrane potential)surrogate
Nicorandil inhibits oxidative stress-induced apoptosis in cardiac myocytes via activation of mitochondrial ATP-sensitive potassium channels.
Cite This Study
Akao et al. (2002) studied Myocardial apoptosis. Nicorandil vs. Hydrogen peroxide alone was evaluated on Apoptotic cell death markers (TUNEL positivity, cytochrome c translocation, caspase-3 activation, and dissipation of mitochondrial inner membrane potential). Nicorandil (100 microM) suppressed markers of apoptosis induced by oxidative stress in cultured cardiac myocytes, an effect blocked by the mitoK(ATP) channel antagonist 5-hydroxydecanoate.