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三氧化二砷抑制淋巴瘤细胞株血管内皮生长因子表达的研究 被引量:1

Znhibition effect of arsenic trioxide on expression of VEGF in lymphoma cell line
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摘要 目的探讨三氧化二砷(ATO)对人类淋巴瘤细胞株内血管内皮生长因子(VEGF)表达的影响。方法应用实时荧光定量聚合酶链(Real-timePCR)技术及酶联免疫吸附(ELISA)法检测ATO作用前后淋巴瘤细胞株Raji及Jurkat内VEGF基因及其蛋白表达量的变化。结果在ATO诱导淋巴瘤细胞株凋亡过程中,两种细胞未经ATO处理前均高表达VEGF mRNA(Raji加药2Ixmol/L12hAACt值0.754±0.15,Jurkat加药3.5[xmol/L72h△△Ct值1.674±0.13)及VEGF蛋白(加药12h,Raji198.384±4.37;Jurkat 563.114±3.81),且Jurkat细胞较Raji细胞的VEGF蛋白的表达量高;经ATO作用24、48、72h后VEGF的mRNA表达量均较加药前明显减少(加药72h△ACt值,Raji:8.954±0.38;Jurkat:9.094±0.16),差异有统计学意义(t=3.54,P〈0.01;t=3.65,P〈0.01);同时蛋白表达量也较加药前明显减少(加药72h,Raji:23.554±2.06;Jurkat:57.11±3.88),差异有统计学意义(t=2.48,P〈0.05;t=2.59,P〈0.05),且两者与药物作用时间明显相关,各时间点之间蛋白表达量差异均有统计学意义(F=2.47,P〈0.05;F=2.50,P〈0.05)。结论ATO通过阻断淋巴瘤细胞生长所需的血管条件,从而抑制淋巴瘤细胞的增殖。 Objective To investigate the effect of arsenic trioxide on expression VEGF of lymphoma cells. Methods The VEGF mRNA expression was analysed by by Real-time PCR, and VEGF protein expression in Raji and Jurkat lymphoma cell lines by ELISA. Results ATO can inhibit lymphoma cells by inducing apoptosis. ATO induced lymphoma cell apoptosis was due to time.With the period of ATO effecting on cells goes, the expression of VEGF mRNA and the protein were down-regulated significantly (after 24, 48, 72 h). There were, the VEGF mRNA△△Ct data of treated with ATO, at 12 h, for Rail: 0.75±0.15, 72 h, Jnrkat: 1.67±0.13. After 72 h, Raji: 8.95±0.38; Jnrkat: 9.09±0.16 (t =3.54, P 〈0.01; t =3.65, P 〈0.01). And about the VEGF protein, at 12 h, Rail: 198.38_+4.37; Jurkat: 563.11±3.81. After 72 h, Rail: 23.55±2.06; Jurkat: 57.11±3.88 (t =2.48, P 〈0.05; t=2.59, P 〈0.05). Conclusion ATO can inhibit the proliferation of lymph oma cells by down-regulating the expression of VEGF mRNA and its protein.
作者 钟璐 徐菲 钟华 王海嵘 钟济华 陈芳源 ZHONG Lu, XU fei, ZHONG Hua, WANG Hai-rong, ZHONG Ji-hua, CHEN Fang-yuan. Department of Hematology, Renji Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200001, China
出处 《白血病.淋巴瘤》 CAS 2011年第5期272-274,共3页 Journal of Leukemia & Lymphoma
关键词 淋巴瘤 肿瘤 实验性 三氧化二砷 血管内皮生长因子类 聚合酶链反应 Lymphoma Neoplasms, experimental Arsenic trioxide Vascular endothelial growthfactors Polymerase chain, reaction
作者简介 通信作者:陈芳源,Email:chenfv04@yah00.com.cn
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  • 1Soignet SL, Maslak P, Wang ZG, et al. Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide. N Engl J Med, 1998, 339: 1341-1348. 被引量:1
  • 2Schroder K, Kirch C, Flasshove M, et al. Constitutive overexpression of the cytidine deaminase gene confers resistance to cytosine arabinoside in vitro. Leukemia, 1996: 1919-1924. 被引量:1
  • 3Mansson E, Liliemark E, Soderhall S, et al. Real-time quantitative PCR assays for deoxcytidine kinase, deoxyguanosine kinase and 5'-nucleotidase mRNA measurement in cell lines and in patients with leukemia. Leukemia, 2002, 16: 386-392. 被引量:1
  • 4Livak KJ, Sehmittqen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2-A ACT method. Methods, 2001, 25: 402-408. 被引量:1
  • 5Roboz GJ, Dias S, Lam G, et al. Arsenic trioxide induces dose-and time-dependent apoptosis of endothelium and may exert an antileukemic effect via inhibition ofangiogenesis. Blood, 2000, 96: 1525-1530. 被引量:1
  • 6Godzich M, Hodnett M, Frank JA, et al. Activation of the stress protein response prevents the development of pulmonary edema by inhibiting VEGF cell signaling in a model of lung ischemia-reperfusion injury in rats. Blood,2006, 2: 1519-1521. 被引量:1

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