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131I-rituximab对B细胞淋巴瘤细胞生物学效应的实验研究
引用本文:魏莉,罗荣城,张军一,严晓,方永鑫,费丽华. 131I-rituximab对B细胞淋巴瘤细胞生物学效应的实验研究[J]. 南方医科大学学报, 2006, 26(2): 211-213
作者姓名:魏莉  罗荣城  张军一  严晓  方永鑫  费丽华
作者单位:南方医科大学南方医院肿瘤中心,广东,广州,510515;南方医科大学南方医院肿瘤中心,广东,广州,510515;南方医科大学南方医院肿瘤中心,广东,广州,510515;南方医科大学南方医院肿瘤中心,广东,广州,510515;南方医科大学南方医院肿瘤中心,广东,广州,510515;南方医科大学南方医院肿瘤中心,广东,广州,510515
摘    要:目的 研究^131Ⅰ标记的rituximab对CD20高表达的B细胞淋巴瘤细胞的生物学效应,为放射免疫导向治疗提供实验依据。方法 IODO—GEN法将^131Ⅰ标记于抗CD20单抗rituximab,用AnnexinV—FITC/PI双染法检测^131Ⅰ-rituximab对Raji细胞的诱导凋亡作用,PI染色法检测细胞周期分布。结果 AnnexinV—FITC/PI双染法检测凋亡率:^131Ⅰ-rituximab组凋亡率为51.99%,^131Ⅰ组为42.71%.rituximab组为29.42%,对照组为26.17%。对照组和rituximab组凋亡率明显低于^131Ⅰ组和^131Ⅰ—rituximab组(P〈0.05)。PI染色法对比各组的凋亡率(亚二倍体峰):^131ⅠI-rituximab组细胞凋亡率为4.32%,^131Ⅰ组为1.47%,rituximab组为1.39%,对照组仅0.37%,^131Ⅰ-rituximab组凋亡率明显高于其他各组(P〈0.05)。^131Ⅰ-rituximab组Raji细胞周期发生变化,细胞大部分被阻滞于G1/G2期。结论 ^131Ⅰ-rituximab能够调控Raji细胞的细胞周期并诱导其凋亡,从而抑制Raji细胞增殖。

关 键 词:B细胞淋巴瘤  放射免疫治疗  碘放射性同位素  rituximab  Raji细胞  细胞凋亡
文章编号:1673-4254(2006)02-0211-03
收稿时间:2005-10-11
修稿时间:2005-10-11

Biological response of B-cell lymphoma cells in vitro to 131I-rituximab
WEI Li,LUO Rong-cheng,ZHANG Jun-yi,YAN Xiao,FANG Yong-xin,FEI Li-hua. Biological response of B-cell lymphoma cells in vitro to 131I-rituximab[J]. Journal of Southern Medical University, 2006, 26(2): 211-213
Authors:WEI Li  LUO Rong-cheng  ZHANG Jun-yi  YAN Xiao  FANG Yong-xin  FEI Li-hua
Affiliation:Center of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Abstract:Objective To study the biological response of B-cell lymphoma cells positive for CD20 expression to 131I-labeled rituximab. Methods Anti-CD20 monoclonal antibody rituximab was labeled with 131I by means of IODO-GEN method, and its effects on apoptosis of Raji cells were determined by Annexin-V/PI double-labeled cytometry. Its effects on the cell cycles was evaluated by cytometry with PI staining. Results The cell apoptosis rate measured by Annexin V-FITC/PI was 51.99% in 131I-rituximab group, significantly higher than that in 131I group, rituximab group and control group (42.71%, 29.42% and 26.17%, respectively, P<0.05). The apoptosis rate by flow cytometry with PI staining was 4.32% in 131I-rituximab group, also significantly higher than that in the other 3 groups (1.47%, 1.39% and 0.37%, respectively, P<0.05). Cell cycle alteration of Raji cells occurred in 131I-rituximab group, and the majority of cells were arrested at G1/G2 stage. Conclusion 131I-rituximab can regulate the cell cycle of Raji cells and induce their apoptosis to inhibit their proliferation.
Keywords:rituximab
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