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机构地区:[1]重庆医科大学分子医学与肿瘤研究中心病理学教研室,重庆400016
出 处:《中国生物制品学杂志》2011年第1期48-51,共4页Chinese Journal of Biologicals
摘 要:目的 探讨抗坏血酸与乳腺癌MDA-MB-231细胞增殖和凋亡的相关性。方法分别用0.5、1.0、2.0和4.0mmol/L的抗坏血酸处理MDA-MB-231细胞,MTT法检测细胞增殖水平;RT-PCR检测细胞p53和bcl-2基因mRNA的转录水平;West-ern blot检测细胞P53和bcl-2蛋白的表达;流式细胞术检测细胞的凋亡率。结果不同浓度的抗坏血酸均可明显抑制MDA-MB-231细胞增殖,促进其凋亡,并使细胞p53基因mRNA转录水平及P53蛋白的表达水平明显升高,而bcl-2基因mRNA转录水平及bcl-2蛋白表达水平明显降低,且均呈剂量依赖性。结论抗坏血酸能抑制MDA-MB-231细胞增殖,诱导其凋亡,其机制可能是通过上调P53,下调bcl-2介导的。Objective To investigate the relationship of ascorbic acid to proliferation and apoptosis of breast cancer MDA-MB-231 cells.Methods MDA-MB-231 cells were treated with ascorbic acid at concentrations of 0.5,1.0,2.0 and 4.0 mmol / L ascorbic acid respectively,then determined for proliferation level by MTT method,for transcription levels of p53 and bcl-2 mRNAs by RT-PCR,for expressions of P53 and bcl-2 proteins by Western blot,and for apoptosis rate by flow cytometry.Results The ascorbic acid at various concentrations inhibited the proliferation and promoted the apoptosis of MDA-MB-231 cells significantly,while increased the transcription level of p53 mRNA and the expression level of P53 protein and decreased the transcription level of bcl-2 mRNA and the expression level of bcl-2 protein,both in dose-dependent modes.Conclusion Ascorbic acid inhibited the pro-liferation and induced the apoptosis of MDA-MB-231 cells in mediation of a potential mechanism of up-regulating P53 and down-regu-lating bcl-2.
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