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[2-甲氧基雌二醇上调Bax/BCL-2比值诱导淋巴瘤Raji细胞凋亡]

[Up-Regulation of Bax/BCL-2 Ratio by 2-Methoxyestradiol Induces Apoptosis in Lymphoma Raji Cells].

作者信息

Zhang Xue-Ya, Guo Xi-Zhe, Wu Shi-Xin

机构信息

Department of Hematology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.

Department of Hematology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China,E-mail:

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2021 Apr;29(2):489-493. doi: 10.19746/j.cnki.issn.1009-2137.2021.02.028.

Abstract

OBJECTIVE

To investigate the effect of 2-methoxyestradiol (2-ME2) to lymphoma Raji cells and its mechanism.

METHODS

Different concentrations of 2-ME2 were used to treat lymphoma Raji cells. CCK8 method was used to detect the effect of 2-ME2 to proliferation of Raji cells. Flow cytometry FITC/PI double labeling method was used to detect early apoptosis of the cells. Western blotting was used to detect the effect of 2-ME2 to the expression of BCL-2, Bax, Caspase-3 and C-myc proteins in Raji cells.

RESULTS

2-ME2 significantly inhibited the proliferation of Raji cells. The inhibition rate increased with the increasing of drug concentration, and increased significantly with the prolongation of drug treatment time (r=0.9215). Flow cytometry FITC/PI double staining showed that the apoptotic rate of 2.5 μmol/L 2-ME2 treatment group was (33.79±1.63) %, while the apoptosis rate of the 48 h group was (51.90±2.72) %, and that of the control group was (7.08±0.36) %. After treated with 2.5 μmol/L 2-ME2 for 12 h, the expression of Bax protein was up-regulated, BCL-2 protein was down-regulated, caspase-3 protein expression was up-regulated, and C-myc protein expression was down-regulated, all of them showed a time-dependent relationship.

CONCLUSION

2-ME2 shows obvious inhibitory effect on lymphoma Raji cells in a dose- and time-dependent manner. Its mechanism of treatment on lymphoma Raji cells may be related to up-regulation of Bax/BCL-2 ratio and activation of Caspase-3 to induce apoptosis in cancer cells. Down-regulation of C-myc protein expression also participates in the apoptotic process.

摘要

目的

探讨2-甲氧基雌二醇(2-ME2)对淋巴瘤Raji细胞的作用及其机制。

方法

采用不同浓度的2-ME2处理淋巴瘤Raji细胞。采用CCK8法检测2-ME2对Raji细胞增殖的影响。采用流式细胞术FITC/PI双标记法检测细胞早期凋亡情况。采用蛋白质免疫印迹法检测2-ME2对Raji细胞中BCL-2、Bax、Caspase-3和C-myc蛋白表达的影响。

结果

2-ME2显著抑制Raji细胞的增殖。抑制率随药物浓度的增加而升高,随药物作用时间的延长而显著升高(r=0.9215)。流式细胞术FITC/PI双染显示,2.5 μmol/L 2-ME2处理组的凋亡率为(33.79±1.63)%,48 h组的凋亡率为(51.90±2.72)%,对照组的凋亡率为(7.08±0.36)%。用2.5 μmol/L 2-ME2处理12 h后,Bax蛋白表达上调,BCL-2蛋白表达下调,caspase-3蛋白表达上调,C-myc蛋白表达下调,均呈时间依赖性关系。

结论

2-ME2对淋巴瘤Raji细胞具有明显的剂量和时间依赖性抑制作用。其对淋巴瘤Raji细胞的治疗机制可能与上调Bax/BCL-2比值、激活Caspase-3诱导癌细胞凋亡有关。C-myc蛋白表达下调也参与了凋亡过程。

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