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绿原酸对人胶质瘤细胞U251的抗肿瘤活性及其促凋亡机制

Anti-tumor Effects of Chlorogenic Acid on Human Glioblastoma Cell Lines U251 and Related Pro-apoptotic Mechanism

  • 摘要:
    目的 研究绿原酸对人胶质瘤细胞U251细胞株增殖、凋亡的作用及其机制。
    方法 培养人胶质瘤U251细胞,不同浓度绿原酸处理细胞48 h后,CCK-8法检测细胞生长抑制率,观察细胞形态学变化;Annexin V-FITC/PI染色法检测细胞凋亡,RT-PCR及Western blot检测p53、Livin、Bcl-2、Bax mRNA和蛋白的表达,Western blot检测Caspase-3蛋白的表达。
    结果 不同浓度绿原酸干预U251细胞48 h后显著抑制细胞的增殖活性,促进细胞凋亡,并且能够上调p53和Bax基因,下调Livin、Bcl-2 mRNA和蛋白的表达,促进Caspase-3蛋白的表达。
    结论 绿原酸可能是通过上调p53和Bax的表达,下调Livin和Bcl-2的表达,激活Caspase-3蛋白,最终诱导U251细胞凋亡。

     

    Abstract:
    Objective To investigate the effects and mechanism of chlorogenic acid (CGA) on the proliferation and apoptosis of human glioma cell line U251.
    Methods Human glioma U251 cells were treated with different concentrations of chlorogenic acid for 48h,then CCK-8 was used to detect the inhibitory rate of cell growth. Annexin V-FITC/PI staining assay was used to detect the apoptosis. RT-PCR and Western blot were used to measure the mRNA and protein levels of p53,Livin,Bcl-2 and Bax,and the protein level of Caspase-3 was detected by Western blot.
    Results Different concentrations of chlorogenic acid significantly inhibited the proliferation of U251 cells and promoted the apoptosis. Chlorogenic acid could up-regulate the expression of p53,Bax and down-regulate the expression of Livin,Bcl-2 at mRNA and protein levels,and increase the protein level of Caspase-3.
    Conclusion CGA could inhibit the proliferation and induce the apoptosis of U251 cells via up-regulating p53 and Bax expression,down-regulating Livin and Bcl-2 expression,and activating Caspase-3 protein.

     

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