Role of TLR4/MyD88/NF-κB signaling pathway in coronary microembolization-induced myocardial injury prevented and treated with nicorandil - 25/08/18
, Xiangwei Lv a, Yuhan Sun b, Ziliang Ye b, Binghui Kong b, Zhenbai Qin bBienvenue sur EM-consulte, la référence des professionnels de santé.
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| pages | 9 |
| Iconographies | 11 |
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Graphical abstract |
Highlights |
• | Myocardial inflammation occurred after CME and caused myocardial injury and a decline of cardiac function. |
• | Nicorandil pretreatment effectively inhibited myocardial inflammation and ameliorated myocardial injury in the CME rat model. |
• | Nicorandil ameliorated LPS-induced myocardial inflammation and enhanced the viability of the cardiomyocytes. |
• | Nicorandil inhibited TLR4/MyD88/NF-κB signaling to achieve myocardial protection. |
Abstract |
Coronary microembolization (CME) is a common complication during the treatment of acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI). Nicorandil can be used to prevent myocardial injury after PCI to reduce the incidence of coronary no-reflow and slow flow, and play a role in myocardial protection, suggesting that its mechanism may be related to the inhibition of CME-induced inflammation of cardiomyocytes. However, the specific mechanism remains unclear. This study investigated the myocardial protective effects of nicorandil pretreatment on CME-induced myocardial injury and the specific mechanism of its inhibition of myocardial inflammation. An CME rat model exhibited CME-induced myocardial inflammation and the elevation of serum tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β based on echocardiography, myocardial enzyme detection, hematoxylin and eosin (HE) and hematoxylin-basic fuchsin-picric acid (HBFP) stainings, ELISA, quantitative real-time PCR, and western blotting. Nicorandil treatment seven days before CME induction effectively inhibited myocardial inflammation, ameliorated myocardial injury, and improved cardiac function, mainly by inhibiting Toll-like receptor 4 (TLR4)-mediated myeloid differentiation primary response protein 88 (MyD88)-dependent nuclear factor-kappa B (NF-κB) signaling. Rat neonatal cardiomyocyte experiments further confirmed that nicorandil ameliorated lipopolysaccharide (LPS)-induced myocardial inflammation and improved cardiomyocyte survival. The specific mechanisms mainly involved the inhibition of TLR4/MyD88/NF-κB signaling and the reduction of the inflammatory cytokines TNF-α and IL-1β released from cardiomyocytes. In summary, nicorandil significantly protected cardiomyocytes from CME-induced myocardial injury mainly by inhibiting TLR4/MyD88/NF-κB signaling, thereby reducing the onset of CME-induced myocardial inflammation. This could be one of the important mechanisms for reducing postoperative myocardial injury via PCI-preoperative prophylactic treatment with nicorandil.
Le texte complet de cet article est disponible en PDF.Keywords : Nicorandil, Coronary, Microembolization, Myocardial Injury, Inflammation, TLR4/MyD88/NF-κB signaling pathway
Plan
Vol 106
P. 776-784 - octobre 2018 Retour au numéro
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