Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel
详细信息 查看全文
- 作者：Reza Badalzadeh (1) (2) (3)
Bahman Yousefi (3) (4)
Maryam Majidinia (4)
Hadi Ebrahimi (1) - 关键词：Arrhythmia ; Diosgenin ; Ischemia–reperfusion ; Myocardial infarction ; Nitric oxide ; Mitochondrial KATP Channel
- 刊名：The Journal of Physiological Sciences
- 出版年：2014
- 出版时间：November 2014
- 年：2014
- 卷：64
- 期：6
- 页码：393-400
- 全文大小：461 KB
- 参考文献：1. Perrelli MG, Pagliaro P, Penna C (2011) Ischemia/reperfusion injury and cardioprotective mechanisms: role of mitochondria and reactive oxygen species. World J Cardiol 3:186-00 CrossRef
2. Murphy E, Steenbergen C (2008) Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol Rev 88:581-09 CrossRef
3. Murry CE, Jennings RB, Reimer KA (1986) Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74:1124-136 CrossRef
4. Keeley EC, Boura JA, Grines CL (2003) Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet 361:13-0 CrossRef
5. Burwell LS, Brookes PS (2008) The cardioprotective effects of nitric oxide in ischemia-reperfusion injury. Antioxid Redox Signal 10:579-00 CrossRef
6. Avkiran M, Ibuki C (1992) Reperfusion-induced arrhythmias: a role for washout of extracellular protons? Circ Res 71:1429-440 CrossRef
7. Matejikova J, Kucharska J, Pinterova M, Pancza D, Raninjerova T (2009) Protection against ischemia-induced ventricular arrhythmias and myocardial dysfunction conferred by preconditioning in the rat heart: involvement of mitochondrial K(ATP) channels and reactive oxygen species. Physiol Res 58:9-9
8. Di Lisa F, Canton M, Menabó R, Kaludercic N, Bernardi P (2007) Mitochondria and cardioprotection. Heart Fail Rev 12:249-60 CrossRef
9. Grover GJ, Atwal KS, Sleph PG, Wang FL, Monshizadegan H, Monticello T, Green DW (2004) Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity. Am J Physiol Heart Circ Physiol 287:H1747–H1755 CrossRef
10. Ardehali H (2004) Role of the mitochondrial ATP-sensitive K+ channels in cardioprotection. Acta Biochim Pol 51:379-90
11. Jin C, Wu J, Watanabe M, Okada T, Iesaki T (2012) Mitochondrial K+ channels are involved in ischemic postconditioning in rat hearts. J Physiol Sci 62:325-32 CrossRef
12. Ma H, Huang X, Li Q, Guan Y, Yuan F, Zhang Y (2011) ATP-dependent potassium channels and mitochondrial permeability transition pores play roles in the cardioprotection of theaflavin in young rat. J Physiol Sci 61:337-42 CrossRef
13. Jin C, Sonoda S, Fan L, Watanabe M, Kugimiya T, Okada T (2009) Sevoflurane and nitrous oxide exert cardioprotective effects against hypoxia-reoxygenation injury in the isolated rat heart. J Physiol Sci 59:123-29 CrossRef
14. Andelová E, Barteková M, Pancza D, Styk J, Ravingerová T (2005) The role of NO in ischemia/reperfusion injury in isolated rat heart. Gen Physiol Biophys 24:411
15. Dana A, Baxter CF, Yellon DM (2001) Delayed or second window preconditioning induced by adenosine A1 receptor activation is independent of early generation of nitric oxide or late induction of inducible nitric oxide synthase. J Cardiovasc Pharmacol 38:278-87 CrossRef
16. Ferdinandy FP, Schulz R (2003) Nitric oxide, superoxide, and peroxynitrite in myocardial ischaemia-reperfusion injury and preconditioning. Br J Pharmacol 138:532-43 CrossRef
17. Esfandiarei M, Lam J, Abdoli Yazdi S, Kariminia A, Navarro Dorado J (2010) Diosgenin modulates vascular smooth muscle cell function by regulating cell viability, migration, and calcium homeostasis. J Pharmacol - 作者单位：Reza Badalzadeh (1) (2) (3)
Bahman Yousefi (3) (4)
Maryam Majidinia (4)
Hadi Ebrahimi (1)
1. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
2. Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
3. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
4. Students-Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran - ISSN：1880-6562
文摘
This study was designed to investigate the anti-arrhythmic effect of diosgenin preconditioning in myocardial reperfusion injury in rat, focusing on the involvement of the nitric oxide (NO) system and mitochondrial ATP-dependent potassium (mitoKATP) channels in this scenario. After isolation of the hearts of male Wister rats, the study was conducted in an isolated buffer-perfused heart model. Global ischemia (for 30 min) was induced by interruption of the aortic supply, which was followed by 90-min reperfusion. Throughout the experiment, the electrocardiograms of hearts were monitored using three golden surface electrodes connected to a data acquisition system. Arrhythmias were assessed based on the Lambeth convention and were categorized as number, duration and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular complexes (PVC), and arrhythmic score. Additionally, lactate dehydrogenase (LDH) levels in coronary effluent were estimated colorimetrically. Diosgenin pre-administration for 20?min before ischemia reduced the LDH release into the coronary effluent, as compared with control hearts (P?ATP channels using 5-hydroxydecanoate as well as inhibiting the NO system through prior administration of l-NAME significantly reduced the positive effects of diosgenin. Our finding showed that pre-administration of diosgenin could provide cardioprotection through anti-arrhythmic effects against ischemia–reperfusion (I/R) injury in isolated rat hearts. In addition, mitoKATP channels and NO system may be the key players in diosgenin-induced cardioprotective mechanisms.