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白藜芦醇对阿霉素致淋巴瘤裸鼠颈动脉内皮细胞凋亡的拮抗作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第5期
页码:
565-568，582
栏目:
基础研究
出版日期:
2012-10-25

文章信息/Info

Title:
Protective effect of resveratrol on doxorubicin-induced artery endothelial apoptosis in lymphoma model of nude mice
作者:
顾 俊1; 胡 伟1; 宋芝萍1; 陈跃光1; 刘 旭2; 张大东1
(1.上海瑞金医院集团闵行区中心医院心内科，上海 201100；
2.上海交通大学附属胸科医院心内科，上海 200030)
Author(s):
GU Jun1;  HU Wei1;  SONG Zhi-ping1;  CHEN Yue-guang1;  LIU Xu2;  ZHANG Da-dong1
(1.Department of Cardiology, Shanghai Minhang District Central Hospital, Ruijin Hospital Group, Shanghai 201100, China; 2.Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 201100, China)
关键词:
白藜芦醇; 阿霉素; 内皮细胞; 凋亡; 淋巴细胞瘤; 裸鼠
Keywords:
resveratrol;  doxorubixin;  endothelial cell;  apoptosis;  lymphoma;  nude mouse
分类号:
R392.2
DOI:
-
文献标识码:
A
摘要:
目的:探讨白藜芦醇(RES)在阿霉素(DOX)所致淋巴瘤裸鼠动脉内皮细胞凋亡中的拮抗作用及相关机制。方法： 给30只雄性Balb/c裸鼠经皮下接种Raji细胞建立淋巴瘤模型并随机分成3组，即对照组、DOX组和DOX+RES组，每组10只(n=10)。用分光光度法测定颈动脉组织中半胱氨酸蛋白酶3(Caspase 3)的活性。用免疫组化染色法检测颈动脉组织中诱导型一氧化氮合酶(iNOS)、Bcl-2和Bax的表达。应用TUNEL方法检测颈动脉内皮细胞的凋亡。分别予以Western blot和硝酸还原酶方法检测淋巴瘤裸鼠颈动脉组织中iNOS蛋白的表达和血清中NO的含量。结果： 与DOX组相比较，DOX+RES组颈动脉组织中iNOS的表达下调（P<0.05），血清NO的含量减少（P<0.01），Bcl-2的表达升高（P<0.01），Bax的表达降低（P<0.01），Caspase 3的活性明显降低（P<0.01），颈动脉内皮细胞凋亡的数量明显减少（P<0.01）。DOX+RES组和DOX组的移植肿瘤的体积无明显差异。结论： RES对于DOX所致淋巴瘤裸鼠动脉内皮细胞凋亡具有拮抗作用，其作用机制可能涉及抑制iNOS/NO途径。
Abstract:
AIM:To study the effect of resveratrol (RES) on doxorubicin (DOX)-induced artery endothelial apoptosis in lymphoma model of nude mice and associated mechanisms. METHODS: Raji cells were injected subcutaneously to develop the lymphoma model in 30 Balb/c nude mice. Thirty lymphoma models were randomly divided into three groups: group 1 (n=10) as control group, group 2 (n=10) as DOX group and group 3 (n=10) as DOX+RES group. Caspase 3 activity of carotid artery tissue was determined by spectrophotometry. iNOS, Bcl-2 and Bax protein expressions in carotid artery were detected by immunohistochemisty and endothelial apoptosis of the carotid artery was evaluated by TUNEL assay. Furthermore, iNOS protein expression of carotid artery and NO formation of serum were determined by Western blot and nitrate reductase, respectively. RESULTS: Protein expression of iNOS (P<0.05) and NO (P<0.01) level in DOX+RES group were inhibited compared with those in DOX group. In DOX+RES group, Bcl-2 expression was higher (P<0.01), Bax expression was lower (P<0.01), and caspase 3 activity was significantly lower (P<0.01) than in the DOX group. TUNEL assay showed less endothelial cell apoptosis in DOX+RES group compared with those in DOX group (P<0.01). No difference in tumor volume was found between DOX+RES group and DOX group (P>0.05). CONCLUSION: RES has protective effects against doxorubicin-induced artery endothelial cell apoptosis in lymphoma model of nude mice, which may be associated with its inhibitory effect on iNOS/NO pathway.

参考文献/References

[1]Chow AY,Chin C,Dahl G,et al.Anthracyclines causes endothelial injury in pediatric cancer patients: a pilot study[J].J Clin Oncol,2006,24(6):925-928.
[2]Wu S,Ko Y,Teng M,et al.Adriamycin-induced cardiomyocytes and endothelial cell apoptosis:in vitro and vivo studies[J].J Cell Moll Cardiol,2002,34(12):1595-1607.
[3]Alpsoy S,Uygur R,Aktas C,et al.The effects of onion (Allium cepa) extract on doxorubicin-induced apoptosis in aortic endothelial cells[J].J Appl Toxicol, 2011 Oct 12.doi: 10.1002/jat.1750.[Epub ahead of print]
[4]Kinlay S,Libby P,Ganz P.Endothelial function and coronary artery disease[J].Curr Opin Lipidol,2001,12(4):383-389.
[5]Das S,Alagappan VK,Bagchic D,et al.Coordinated induction of iNOS-VEGF-KDR-eNOS after resveratrol consumption:a potential mechanism for resveratrol preconditioning of the heart[J].Vascul Pharmacol,2005,42(5-6):281-289.
[6]Zou JG,Huang YZ,Cao KJ,et al.Effect of resveratrol on intimal hyperplasia after endothelial denudation in an experimental rabbit model[J].Life Sciences,2000,68(2):153-163.
[7]Fukuda S,Kaga S,Zhan L,et al.Resveratrol ameliorates myocardial damage by inducing vascular endothelial growth factor-angiogenesis and tyrosine kinase receptor Flk-1[J].Cell Biochem Biophys,2006,44(1):43-49.
[8]Kaga S,Zhan L,Matsumoto M,et al.Resveratrol enhances neovas-cularization in the infarcted rat myocardium through the induction of thioredoxin-1, heme oxygenase-1 and vascular endothelial growth factor[J].J Moll Cell Cardiol,2005, 39(5):813-822.
[9]Olukman M,Can C,Erol A,et al.Reversal of doxorubicin-induced vascular dysfunction by resveratrol in rat thoracic aorta: Is there a possible role of nitric oxide synthase inhibition?[J].Anadolu Kardiyol Derg,2009,9(4):260-266.
[10]金 贤，冯小弟，胡 伟，等.年轻恶性淋巴瘤患者并发急性心梗一例[J].上海交通大学学报（医学版）,2008,28(3):353-354.
[11]Zhou S,Starkov A,Froberg MK,et al.Cumulative and irreversible cardiac mitochondrial dysfunction induced by doxorubicin[J].Cancer Res,2001,61(2):771-777.
[12]Childs AC,Phaneuf SL,Dirks AJ,et al.Doxorubicin treatment in vivo causes cytochrome C release and cardiomyocyte apoptosis as well as increased mitochondrial efficiency,superoxid dismutase activity,and Bcl-2: Bax ratio[J].Cancer Res, 2002,62(16):4592-4598.

备注/Memo

备注/Memo:
收稿日期：2012-04-27.
基金项目：上海市卫生局青年科研项目资助（2008Y052）
通讯作者：张大东，主任医师，主要从事冠心病基础和临床的研究Email：ocean2003@yahoo.cn
作者简介：顾俊，主治医师，博士生Email：forrestgu@126.com
更新日期/Last Update: 2012-11-16