Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload
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Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload
Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload
中国结合医学杂志(英文版)2011年17卷第4期 页码:283-289
Affiliations:
1. The Laboratory Research Center of Xiyuan Hospital, China Academy of Chinese Medical Sciences,Beijing,China
2. Yunnan Pharmaceutical Institute,Kunming,China
Author bio:
Funds:
Supported by the Major Scientific and Technological Specialized Project for “Significant New Formulation of New Drugs (No. 2009ZX09301, 2009ZX09303-003)”
Li, P., Fu, Jh., Wang, Jk. et al. Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload., Chin. J. Integr. Med. 17, 283–289 (2011). https://doi.org/10.1007/s11655-011-0704-4
Peng Li, Jian-hua Fu, Jing-kun Wang, et al. Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload[J]. Chinese Journal of Integrative Medicine, 2011,17(4):283-289.
Li, P., Fu, Jh., Wang, Jk. et al. Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload., Chin. J. Integr. Med. 17, 283–289 (2011). https://doi.org/10.1007/s11655-011-0704-4DOI:
Peng Li, Jian-hua Fu, Jing-kun Wang, et al. Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload[J]. Chinese Journal of Integrative Medicine, 2011,17(4):283-289. DOI: 10.1007/s11655-011-0704-4.
Extract of Paris polyphylla Simth protects cardiomyocytes from anoxia-reoxia injury through inhibition of calcium overload
摘要
To assess any direct effect of extract of Paris polyphylla Simth (EPPS)
a Chinese plant
on a cardiomyocyte subject to ischemia-reperfusion injury and to further elucidate its protective effect against myocardium ischemia on the cellular level. Neonatal rat cardiomyocytes were isolated and subjected to an anoxia-reoxia injury simulating the ischemia-reperfusion injury in vivo in the presence or absence of EPPS or diltizem
a positive control. The lactate dehydrogenase (LDH) activities in culture supernatants and cell viabilities were analyzed using the enzymatic reaction kinetics monitoring-method and MTT method
respectively. Free intracellular calcium concentrations and activities of Na+-K+ ATPase and Ca2+ ATPase in cells were also measured with laser confocal microscopy and the inorganic phosphorus-transformation method
respectively. In cardiomyocytes subject to anoxia-reoxia injury
EPPS at 50–400 mg/L showed a concentration-dependent inhibition on LDH leakage and maintenance of cell viability
and the effect was significant at 275 and 400 mg/L (both P<0.01). In addition
EPPS at 275 and 400 mg/L significantly inhibited the increase in intracellular free calcium (both P<0.01) as well as decreased the activities of Na+-K+ ATPase and Ca2+ ATPase (P<0.01
P<0.05). EPPS prevents anoxia-reoxia injury in neonatal rat cardiomyocytes in vitro by preservation of Na+-K+ ATPase and Ca2+ ATPase activities and inhibition of calcium overload. The direct protective effect on cardiomyocytes may be one of the key mechanisms that underlie the potential therapeutic benefit of EPPS against myocardium ischemia.
Abstract
To assess any direct effect of extract of Paris polyphylla Simth (EPPS)
a Chinese plant
on a cardiomyocyte subject to ischemia-reperfusion injury and to further elucidate its protective effect against myocardium ischemia on the cellular level. Neonatal rat cardiomyocytes were isolated and subjected to an anoxia-reoxia injury simulating the ischemia-reperfusion injury in vivo in the presence or absence of EPPS or diltizem
a positive control. The lactate dehydrogenase (LDH) activities in culture supernatants and cell viabilities were analyzed using the enzymatic reaction kinetics monitoring-method and MTT method
respectively. Free intracellular calcium concentrations and activities of Na+-K+ ATPase and Ca2+ ATPase in cells were also measured with laser confocal microscopy and the inorganic phosphorus-transformation method
respectively. In cardiomyocytes subject to anoxia-reoxia injury
EPPS at 50–400 mg/L showed a concentration-dependent inhibition on LDH leakage and maintenance of cell viability
and the effect was significant at 275 and 400 mg/L (both P<0.01). In addition
EPPS at 275 and 400 mg/L significantly inhibited the increase in intracellular free calcium (both P<0.01) as well as decreased the activities of Na+-K+ ATPase and Ca2+ ATPase (P<0.01
P<0.05). EPPS prevents anoxia-reoxia injury in neonatal rat cardiomyocytes in vitro by preservation of Na+-K+ ATPase and Ca2+ ATPase activities and inhibition of calcium overload. The direct protective effect on cardiomyocytes may be one of the key mechanisms that underlie the potential therapeutic benefit of EPPS against myocardium ischemia.
关键词
Paris polyphylla Simthcardiomyocyteanoxia-reoxia injurycalcium-overloadischemia-reperfusion injury
Keywords
Paris polyphylla Simthcardiomyocyteanoxia-reoxia injurycalcium-overloadischemia-reperfusion injury
references
Shimokawa H, Yasuda S. Myocardial ischemia: current concepts and future perspectives. J Cardiol 2008;52:67–78.
Nie R, Xia R, Zhong X, Xia Z. Salvia miltiorrhiza treatment during early reperfusion reduced postischemic myocardial injury in the rat. Can J Physiol Pharmacol 2007;85:1012–1019.
Wu L, Ling H, Li L, Jiang L, He M. Beneficial effects of the extract from Corydalis yanhusuo in rats with heart failure following myocardial infarction. J Pharm Pharmacol 2007;59:695–701.
Kim TH, Lee SM. The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart. Food Chem Toxicol 2010;48:1516–1520.
Zhao JY. Advance in research of Qiyelian (Paris polyphylla Simth). Guangming Tradit Chin Med (Chin) 2009;24:2224–2226.
Kitakaze M, Asanuma H, Takashima S, Minamino T, Ueda Y, Sakata Y, et al. Nifedipine-induced coronary vasodilation in ischemic hearts is attributable to bradykinin- and NO-dependent mechanisms in dogs. Circulation 2000;101:311–317.
Michiels C. Physiological and pathological responses to hypoxia. Am J Pathol 2004;164:1875–1882.
Frangogiannisa NG, Smith CW, Entmana ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002;53:31–47.
Rakhit RD, Mojet MH, Marber MS, Duchen MR. Mitochondria as targets for nitric oxide-induced protection during simulated ischemia and reoxygenation in isolated neonatal cardiomyocytes. Circulation 2001;103:2617–2623.
Vistica DT, Skehan P, Scudiero D, Monks A, Pittman A, Boyd MR. Tetrazolium-based assays for cellular viability: a critical examination of selected parameters affecting formazan production. Cancer Res 1991;51:2515–2520.
Mizukami Y, Ono K, Du CK, Aki T, Hatano N, Okamoto Y, et al. Identification and physiological activity of survival factor released from cardiomyocytes during ischaemia and reperfusion. Cardiovasc Res 2008;79:589–599.
Kao JP, Harootunian AT, Tsien RY. Photochemically generated cytosolic calcium pulses and their detection by Fluo-3. J Biol Chem 1989;264:8179–8184.
Ruiz-Meana M, Garcia-Dorado D, Pina P, Inserte J, Agulló L, Soler-Soler J. Cariporide preserves mitochondrial proton gradient and delays ATP depletion in cardiomyocytes during ischemic conditions. Am J Physiol Heart Circ Physiol 2003;285:H999–H1006.
Piper HM, Meuter K, Schäfer C. Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg 2003;75:S644–S648.
Carafoli E, Santella L, Branca D, Brini M. Generation, control, and processing of cellular calcium signals. Crit Rev Biochem Mol Biol 2001;36:107–260.
Vila-Petroff M, Salas MA, Said M, Valverde CA, Sapia L, Portiansky E, et al. CaMKII inhibition protects against necrosis and apoptosis in irreversible ischemia-reperfusion injury. Cardiovasc Res 2007;73:689–698.
Halestrap AP, Clarke SJ, Javadov SA. Mitochondrial permeability transition pore opening during myocardial reperfusion—a target for cardioprotection. Cardiovasc Res 2004;61:372–385.
Inserte J, Garcia-Dorado D, Hernando V, Barba I, Soler-Soler J. Ischemic preconditioning prevents calpain-mediated impairment of Na+/K+-ATPase activity during early reperfusion. Cardiovasc Res 2006;70:364–373.
Xie Y, Zhu Y, Zhu WZ, Chen L, Zhou ZN, Yuan WJ, et al. Role of dual-site phospholamban phosphorylation in intermittent hypoxia-induced cardioprotection against ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 2005;288:H2594–H2602.
Cartwright EJ, Schuh, Neyses L. Calcium transport in cardiovascular health and disease—the sarcolemmal calcium pump enters the stage. J Mol Cell Cardiol 2005;39:403–406.
Viola HM, Macdonald WA, Tang H, Hool LC. The L-type Ca2+ channel as a therapeutic target in heart disease. Curr Med Chem 2009;16:3341–3358.
Zima AV, Blatter LA. Redox regulation of cardiac calcium channels and transporters. Cardiovasc Res 2006;71:310–321.