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人参皂苷Rb1对缺氧复氧诱导内皮细胞凋亡的影响 被引量:11

Effect of ginsenoside on endothelial cells apoptosis induced by hypoxia-reoxygenation
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摘要 目的:观察缺氧复氧诱导人脐静脉内皮细胞凋亡现象及人参皂苷Rb1的干预效应。方法:体外培养人脐静脉内皮细胞,建立内皮细胞缺氧复氧模型,采用TUNEL技术和DNA凝胶电泳观察缺氧不同时间(0、3、6、12、24 h)后复氧对内皮细胞凋亡的影响及Rb1的干预效应。结果:随着缺氧时间延长,复氧后脐静脉内皮细胞凋亡率逐渐升高;Rb1组内皮细胞凋亡率显著低于缺氧复氧组(P<0.05)。结论:内皮细胞凋亡是缺氧复氧损伤的一种重要形式,人参皂苷Rb1通过抑制缺氧复氧诱导内皮细胞凋亡而起到内皮细胞保护效应。 Objective:To observe the endothelial cells apoptosis induced by hypoxia and reoxygenation and the inhibiting effect of ginsenoside Rbl. Method: Human umbilical vein endothelial cells (HUVECs) were cultivated and divided into five groups randomly, which were used to establish the hypoxia-reoxygenation models. TUNEI. technology was used to quantify the apoptotic and necrotic cells. DNA electrophoresis was utilized to determine changes characteristic of apoptosis. Result: Percentage of apoptosis in different groups was significantly distinctive, which increased steadily with the duration of hypoxia reoxygenation, apoptic cells in Rbl group were significantly less than in the hypoxia-reoxygenation group ( P〈 0.05). Conclusion: Hypoxia-reoxygenation could initiate apoptosis in cultivated HUVECs in a time dependent manner. Rbl exerts cell protection in hypoxia reoxygenation injury by inhibiting endothelial cells apoptosis.
出处 《临床心血管病杂志》 CAS CSCD 北大核心 2005年第12期728-730,共3页 Journal of Clinical Cardiology
基金 湖北省科技攻关计划重点项目资助(No:2001AA307B03)
关键词 内皮 血管 细胞凋亡 缺氧 人参皂苷 Endothelium,vascular Apoptosis Hypoxia Ginsenoside
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参考文献6

  • 1Li C,Jackson R M.Reactive species mechanisms of cellular hypoxia-reoxygenation injury.Am J Physiol Cell Physiol,2002,282:C227-C241.
  • 2Warren M C,Bump E A,Medeiros D,et al.Oxidative stress-induced apoptosis of endothelial cells.Free Radic Biol Med,2000,29:537-547.
  • 3Jonathan C C,David J G,David W C H.Endothelial cell apoptosis:biochemical characteristics and potential implication for atherosclerosis.J Moll Cell Cardiol,2001,33:1673-1690.
  • 4Scarabelli T,Stephanou A,Rayment R,et al.Apoptosis of endothelial cells precedes myocyte cell apoptosis in ischemia/reperfusion injury.Circulation,2001,104:253-257.
  • 5Zhao H,Miller M,Pfeiffer K,et al.Anoxia and reox ygenation of human endothelial cells decrease ceramide glucosyltransferase expression and activates caspases.Faseb J,2003,17:723-724.
  • 6蓝荣芳,李志刚,刘正湘.人参皂甙Rb_1对大鼠缺血再灌注心肌细胞Bcl-2、Bax、Bad、Fas基因表达的影响[J].中国组织化学与细胞化学杂志,2002,11(2):149-152. 被引量:28

二级参考文献19

  • 1Gottlieb RA,Engler RL.Apoptosis in myocardial ischemia-reperfusion.Ann N Y Acad Sci,1999,874: 412-26
  • 2Strasser A,Harris AW,Jacks T,et al.DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by Bcl-2.Cell,1994,79: 329-39
  • 3Yin XM,Oltvai ZN,Korsmeyer SJ.BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax.Nature,1994,369: 321-3
  • 4Oltvai ZN,Milliman CL,Korsmeyer SJ.Bcl-2 heterodimerizes in vivo with a conserved homolog,Bax,that accelerates programmed cell death.Cell,1993,74: 609-19
  • 5Yang E,Zha J,Jockel J,et al.Bad,a heterodimeric partner for Bcl-XL and Bcl-2,displaces Bax and promotes cell death.Cell,1995,80: 285-91
  • 6Green DR,Reed JC.Mitochondria and apoptosis.Science,1998,281: 1309-12
  • 7Cook SA,Pool-Wilson PA.Cardiac myocyte apoptosis.Eur Heart J,1999,20: 1619-29
  • 8Tanaka MT,Itoh N,Adachi S,et al.Hypoxia induces apoptosis with enhanced expression of Fas antigen messenger RNA in cultured neonatal rat cardiomyocytes.Circ Res,1994,75: 426-33
  • 9Watanabe-fukunaga R,Brannan CI,Itoh N,et al.The cDNA structure,expression,and chromosomal assignment of the mouse Fas antigen.J Immunol,1992,148: 1274-79
  • 10Felzen B,Shilkrut M,Less H,et al.Fas(CD95/APO-1)-mediated damage to ventricular myocytes induced by cytotoxic T lymphocytes from perforin-deficient mice: a major role for inositol1,4,5-triphosphate.Circ Res,1998,82: 438-50

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