| 翟丽娜,翁 翔,黄 强.PI3K/AKt通路参与苦参碱抑制raji细胞增殖与凋亡过程的机制研究[J].中国肿瘤,2015,24(6):517-523. |
| PI3K/AKt通路参与苦参碱抑制raji细胞增殖与凋亡过程的机制研究 |
| The Mechanism of Matrine Inhibits Raji Cells Proliferation and Apoptosis via PI3K/AKt Pathway |
| 投稿时间：2014-10-12 |
| DOI：10.11735/j.issn.1004-0242.2015.06.A017 |
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| 中文关键词: 苦参碱 非霍奇金淋巴瘤 PTEN AKt raji细胞 增殖 凋亡 |
| 英文关键词:Matrine non-hodgkin's lymphoma PTEN AKt raji cells cell proliferation apoptosis |
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| 中文摘要: |
| 摘 要：［目的］探讨苦参碱体外诱导非霍奇金淋巴瘤raji细胞增殖与凋亡的机制是否与PI3K/AKt信号通路有关。［方法］ MTT法检测苦参碱作用后raji细胞的增殖抑制率；流式细胞仪检测苦参碱作用后raji细胞的细胞周期的变化；RT-PCR 检测苦参碱作用后PTEN、AKt、caspase3 等mRNA水平的变化；Western blot检测PTEN、pBad、Bad、pAKt、AKt、caspase3等蛋白的表达。［结果］ 苦参碱可抑制raji细胞的增殖，随着药物浓度的提高和作用时间的延长，细胞的增殖抑制率逐渐升高，与对照组比较，差异均有显著(P<0.001)；苦参碱诱导raji细胞周期停滞于G1期(P<0.05)；苦参碱可通过磷酸化AKt来上调PTEN的表达，引起Bad、p21、p27等的变化，与对照组分别比较表达水平差异均有统计学意义(P<0.05)，最终诱导caspase家族级联反应，引发肿瘤细胞的凋亡。［结论］ 苦参碱可通过PI3K/AKt信号通路抑制非霍奇金淋巴瘤raji细胞的增殖，诱导raji细胞凋亡。 |
| 英文摘要: |
| Abstract：［Purpose］ To investigate the mechanism of the non-hodgkin's lymphoma raji cells proliferation and apoptosis induced by matrine in vitro，and whether that is associated with PI3K/AKt signaling pathways. ［Methods］ The raji cells growth inhibition rate treated with matrine was detected by MTT. The distribution of cell cycles was analyzed by Flow cytometry；further，the mRNA change of the PTEN，AKt and caspase3 was quantified by the real time-PCR and the protein expression of PTEN，pBad，Bad，pAKt，AKt and caspase3 was measured by Western blot. ［Results］ the growth of raji cells inhibited with the increase of drug concentration and the extension of time of Matrine，the cell growth inhibition rate increased(Compared with control，P all<0.001)；Matrine induced the stagnation of the cell cycle in G1 phase(P<0.05)；the expression of PTEN increased by the AKt phosphorylated of Matrine，leading to the change of Bad，p21 and p27，and eventually induced the cascade of caspase family and triggered the apoptosis of tumor cells(compared with control，P all<0.05). ［Conclusion］ Matrine could suppress the non-hodgkin’s lymphoma raji cells proliferation and induce cell apoptosis through PI3K/AKt pathway. |
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