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内皮素-1对缺氧/复氧所致心肌细胞凋亡的影响
引用本文:郭万刚,余志斌,孙立军,罗中华. 内皮素-1对缺氧/复氧所致心肌细胞凋亡的影响[J]. 心脏杂志, 2007, 19(1): 12-15. DOI: 10.13191/j.chj.2007.01.18.guowg.005
作者姓名:郭万刚  余志斌  孙立军  罗中华
作者单位:1. 第四军医大学航空航天医学系航空航天生理学教研室
摘    要:目的探讨在缺氧/复氧过程中不同时期给予内皮素-1(ET-1)对缺氧/复氧所致心肌损伤与凋亡的影响。方法乳鼠心肌细胞缺氧/复氧模型,流式细胞仪检测心肌细胞凋亡,Hoechst 33258染色计算凋亡率,试剂盒检测乳酸脱氢酶(LDH)的活性。结果ET-1预处理组(EP)细胞生存率较缺氧复氧组(HR)提高,凋亡率下降,LDH活性下降;ET-1缺氧即刻处理组(EH)细胞生存率较HR组降低,凋亡率升高,LDH释放量增加;ET-1复氧处理组(ER)的细胞生存率、凋亡率及LDH活性与HR组均无统计学差异。结论ET-1预处理有心肌细胞保护作用,ET-1缺氧时有促进心肌细胞损伤和凋亡的作用。

关 键 词:心肌细胞   缺氧/复氧   细胞凋亡   内皮素-1
文章编号:1009-7236(2007)01-012-04
修稿时间:2005-12-26

Influences of endothelin-1 on apoptosis of hypoxia/reoxygenation myocardiocytes
GUO Wan-gang,YU Zhi-bin,SUN Li-jun,LUO Zhong-hua. Influences of endothelin-1 on apoptosis of hypoxia/reoxygenation myocardiocytes[J]. Chinese Heart Journal, 2007, 19(1): 12-15. DOI: 10.13191/j.chj.2007.01.18.guowg.005
Authors:GUO Wan-gang  YU Zhi-bin  SUN Li-jun  LUO Zhong-hua
Abstract:AIM To explore the effects of endothelin-1 at different administrative timing on apoptosis and cell injury induced by hypoxia/reoxygenation.METHODS Primarily cultured neonatal rat cardiomyctes were treated with 950 ml/L N2-50 ml/L CO2 mixture to establish hypoxia/reoxygenation model. Flow cytometry and Hoechst 33258 stain were performed to determine the apoptotic rates of cardiomyocytes.A domestic kit was used to determine the activity of lactate dehydrogenase(LDH).RESULTS Cell viability values,apoptotic rates and lactate dehydrogenase(LDH) activity of cells with 24 h ET-1 treatment before hypoxia increased,lowered and decreased respectively compared with those in hypoxia/reoxygenation group(HR).ET-1 treatment during hypoxia depressed the cell viability,raised apoptotic rate and LDH release.ET-1 treatment during reoxygenation had no effects on these values.CONCLUSION ET-1 pretreatment has protective effects on cardiomyocytes from hypoxia/reoxygenation.However,ET-1 during hypoxia aggravates the injury of cardiomyocytes induced by hypoxia/reoxygenation.
Keywords:cardiomyocytes  hypoxia/reoxyegenation  apoptosis  endothelin
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