Abstract | BACKGROUND: Coronary microembolization (CME) is a common and intractable complication of coronary revascularization, which leads to perioperative myocardial injury, cardiac dysfunction, and poor prognosis. Nicorandil is widely used for the management of ischemic heart diseases, but the cardioprotective effects of nicorandil beyond anti-angina in CME-induced myocardial injury are worthy of further exploration. Therefore, the present study investigated the effect of nicorandil on CME-induced cardiomyocyte pyroptosis and explored the underlying mechanism. METHODS: RESULTS:
Nicorandil pretreatment attenuated cardiac dysfunction and myocardial injury following CME. Nicorandil also alleviated oxidative stress and mitochondrial damage. Moreover, nicorandil promoted AMPK activation, reduced the expression of thioredoxin-interacting protein (TXNIP), inhibited the activation of the NOD-like receptor pyrin containing 3 (NLRP3) inflammasome, and mitigated cardiomyocyte pyroptosis. However, co-treatment with CC reversed the cardioprotective effects of nicorandil. CONCLUSION:
Nicorandil pretreatment inhibits cardiomyocyte pyroptosis and alleviates CME-induced myocardial injury via the AMPK/TXNIP/NLRP3 signaling pathway.
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Authors | Yangchun Liu, Jin Shu, Tao Liu, Jian Xie, Tao Li, Haoliang Li, Lang Li |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 936
Pg. 175365
(Dec 05 2022)
ISSN: 1879-0712 [Electronic] Netherlands |
PMID | 36336011
(Publication Type: Journal Article)
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Copyright | Copyright © 2022 Elsevier B.V. All rights reserved. |
Chemical References |
- Nicorandil
- AMP-Activated Protein Kinases
- NLR Family, Pyrin Domain-Containing 3 Protein
- TXNIP protein, rat
- Cell Cycle Proteins
- Nlrp3 protein, rat
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Topics |
- Rats
- Animals
- Myocytes, Cardiac
- Nicorandil
(pharmacology, therapeutic use)
- Pyroptosis
- AMP-Activated Protein Kinases
- NLR Family, Pyrin Domain-Containing 3 Protein
- Heart Injuries
- Myocardium
- Signal Transduction
- Myocardial Ischemia
- Cell Cycle Proteins
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