The anti-apoptosis effect of erythropoietin on neonatal rat cardiocytes during hypoxia/reoxygenation injury and its possible mechanism

OBJECTIVE: To investigate the anti-apoptosis effect of erythropoietin (EPO) on myocardial cells after hypoxia/reoxygenation in vitro, and the relationship among protein kinase C (PKC), the mitochondrial ATP-sensitive potassium (mitoKATP) channel and EPO in the anti-apoptotic signaling pathways

Bibliographische Detailangaben
Veröffentlicht in:Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue. - 1998. - 22(2010), 5 vom: 27. Mai, Seite 302-5
1. Verfasser: Wang, Hua-jun (VerfasserIn)
Weitere Verfasser: Jiang, Hui-lin, Chen, Xiao-hui, Lin, Pei-yi, Zhu, Yong-cheng, Tao, Li-li
Format: Aufsatz
Sprache:Chinese
Veröffentlicht: 2010
Zugriff auf das übergeordnete Werk:Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
Schlagworte:English Abstract Journal Article Research Support, Non-U.S. Gov't Potassium Channels mitochondrial K(ATP) channel Erythropoietin 11096-26-7 Protein Kinase C EC 2.7.11.13
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100 1 |a Wang, Hua-jun  |e verfasserin  |4 aut 
245 1 4 |a The anti-apoptosis effect of erythropoietin on neonatal rat cardiocytes during hypoxia/reoxygenation injury and its possible mechanism 
264 1 |c 2010 
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500 |a Citation Status MEDLINE 
520 |a OBJECTIVE: To investigate the anti-apoptosis effect of erythropoietin (EPO) on myocardial cells after hypoxia/reoxygenation in vitro, and the relationship among protein kinase C (PKC), the mitochondrial ATP-sensitive potassium (mitoKATP) channel and EPO in the anti-apoptotic signaling pathways 
520 |a METHODS: Cardiocytes were harvested from neonatal rats and cultured. Cultured myocardial cells were divided into the control group, the hypoxia/reoxygenation group, the EPO group and the chelerythrine group, and a hypoxia/reoxygenation model of cardiocytes was reproduced. Apoptosis rate was assayed by flow cytometry. Flavoprotein fluorescence was scanned by confocal laser microscope to assess the mitoKATP channel activity 
520 |a RESULTS: Apoptosis rate was significantly higher in hypoxia/reoxygenation group than that of control group [(42.56+/-8.00)% vs. (17.88+/-2.00)%, P<0.05]. There was no statistically significant difference in flavoprotein fluorescence between this group and the control group [(0.278+/-0.170)x10(-2) vs. (0.149+/-0.050)x10(-2), P>0.05]. Myocardial cell apoptosis rate in EPO group was lower than that in hypoxia/reoxygenation group [(22.73+/-5.00)% vs. (42.56+/-8.00)%, P<0.05], and flavoprotein fluorescence intensity was significantly enhanced when compared with hypoxia/reoxygenation group [(2.201+/-1.090)x10(-2) vs. (0.278+/-0.170)x10(-2), P<0.01]. However, when chelerythrine was added, the anti-apoptosis effect of EPO was blocked, and the intensity of cardiocytes flavoprotein fluorescence was decreased [the apoptosis rate was (46.72+/-17.00)% and the flavoprotein fluorescence intensity was (0.986+/-0.320)x10(-2) ]. When compared with EPO group there was statistically significant difference (P<0.01 and P<0.05) 
520 |a CONCLUSION: Myocardial cell apoptosis occurs in hypoxia/reoxygenation injury, and EPO can protect rat cardiomyocytes from hypoxia/reoxygenation induced apoptosis. The protective effect is partly associated with the PKC/mitoKATP pathway 
650 4 |a English Abstract 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Potassium Channels  |2 NLM 
650 7 |a mitochondrial K(ATP) channel  |2 NLM 
650 7 |a Erythropoietin  |2 NLM 
650 7 |a 11096-26-7  |2 NLM 
650 7 |a Protein Kinase C  |2 NLM 
650 7 |a EC 2.7.11.13  |2 NLM 
700 1 |a Jiang, Hui-lin  |e verfasserin  |4 aut 
700 1 |a Chen, Xiao-hui  |e verfasserin  |4 aut 
700 1 |a Lin, Pei-yi  |e verfasserin  |4 aut 
700 1 |a Zhu, Yong-cheng  |e verfasserin  |4 aut 
700 1 |a Tao, Li-li  |e verfasserin  |4 aut 
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