陈吉,吴强,韩烨,郭小平,陈敏,蔡运昌,黄岚
CHEN Ji 1; WU Qiang 2; HAN Ye 3; GUO Xiao ping 3; CHEN Min 3; CAI Yun chang 2; HUANG Lan 1 (1 Department of Cardiology;

• 1:第三军医大学附属新桥医院心内科
• 2:贵州省人民医院心内科
• 3:解放军44医院心内科
• 4:解放军44医院心内科

摘要(Abstract)：

目的 :观察不同剂量维生素E对去甲肾上腺素 (NE)诱导心肌细胞肥大的影响。方法 :培养乳鼠心肌细胞暴露于NE(2 0 μmol/L)和维生素E(5 μmol/L ,5 0 μmol/L ,5 0 0 μmol/L) 36h ,检测心肌细胞3 H 亮氨酸掺入率和蛋白质含量的变化。结果 :NE可导致心肌细胞3 H 亮氨酸掺入率和蛋白质含量明显增高 ,5 0 μmol/L ,5 0 0 μmol/L的维生素E干预可抑制NE的致心肌细胞肥大的作用。结论 :NE的促心肌细胞肥大作用可能与活性氧生成增加有关 ,维生素E以剂量依赖方式抑制NE的促肥大作用
Objective: To study the effects of vitamin E of different doses on norepinephrine (NE) induced hypertrophic cardiac myocytes. Methods: After exposed to NE alone (20 μmol/L) and NE+vitamin E (5 μmol/L, 50 μmol/L and 500 μmol/L) for 36 hours, 3H Leucine incorporation and the intracellular content of protein were measured in cultured neonatal rat cardiac myocytes. Results: NE significantly increased 3H Leucine incorporation and the intracellular content of protein. Pretreatment with vitamin E at 50 μmol/L and 500 μmol/L remarkably inhibited NE induced myocardial cell hypertrophy. Conclusion: NE induced cardiomyocyte hypertrophy is associated with overproduction of reactive oxygen species. Vitamin E inhibits the effect of NE in dose dependence.[

关键词(KeyWords)： 维生素E;去甲肾上腺素;肥大;心肌;细胞;大鼠
vitamin E; norepinephrine; hypertrophy; myocardium; cells; rat

Abstract:

Keywords:

基金项目(Foundation): 贵州省科学技术基金资助项目 (30 4 4 ) ;; 贵州省卫生厅科学技术基金资助项目 (1 4 9)

作者(Authors): 陈吉,吴强,韩烨,郭小平,陈敏,蔡运昌,黄岚
CHEN Ji 1; WU Qiang 2; HAN Ye 3; GUO Xiao ping 3; CHEN Min 3; CAI Yun chang 2; HUANG Lan 1 (1 Department of Cardiology;

DOI: 10.19367/j.cnki.1000-2707.2004.01.007

参考文献(References)：

• [1]IzumoS ,AokiH .Calcineurin themissinglinkincardiachy pertrophy[J].NatMed,1998,4(6):661-662.
• [2]李小鹰.心血管疾病分子生物学[M].北京:人民军医出版社,2000.173.
• [3]ChibaM ,ShidaM ,MiyazakiY ,etal.Roleofadrenergicre ceptorsystemincanineleftventricularhypertrophy[J].JMolCellCardiol,1989,21(15):39-47.
• [4]CohenJ .Roleofendocrinefactorsinthepathogenesisofcar diachypertrophy[J].CircRes,1974,35(11):49-57.
• [5]NakamuraK ,FushimiK ,KouchiH ,etal.Inhibitoryeffectsofantipxidantsonneonatalratcardiacmyocytehypertrophyin ducedbytumornecrosisfactor alphaandangiotensin11[J].Circulation,1998,98(8):794-799.
• [6]ChengTH ,ShihNL ,ChenSY ,etal.ReactiveoxygenspeciesmodulateendothelinI inducedc fosgeneexpressionincar diomyocytes[J].CardiovascRes,1999,41(3):654-662.
• [7]AikawaR ,KomuroI ,YamazakiT ,etal.RhofamilysmallGproteinsplaycriticalrolesinmechanicalstress inducedhyper trophicresponsesincardiacmyocytes[J].CircRes,1999,84(4):458-466.
• [8]BellJP ,MosferSI,LangD ,etal.VitaminCandquinaprilab rogateLVHandendothelialdysfunctioninaortic bandedguineapigs[J].AmJPhysiolHeartCircPhysiol,2001,281(4):1704-1710.
• [9]HausseAO ,AggounY ,BonnetD ,etal.Idebenoneandre ducedcardiachypertrophyinFriedreich’sataxia[J].Heart,2002,87(4):346-349.
• [10]BunoutD .TherapeuticpotentialofvitaminEinheartdisease[J].ExpertOpinInvestigDrugs,2000,9(11):2629-2635.

文章评论(Comment)：