首页> 外文期刊>Phytotherapy research: PTR >Fructus ligustri lucidi extracts induce human glioma cell death through regulation of Akt/mTOR pathway in vitro and reduce glioma tumor growth in U87MG xenograft mouse mode
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Fructus ligustri lucidi extracts induce human glioma cell death through regulation of Akt/mTOR pathway in vitro and reduce glioma tumor growth in U87MG xenograft mouse mode

机译:山茱li提取物通过体外调节Akt / mTOR途径诱导人神经胶质瘤细胞死亡,并在U87MG异种移植小鼠模型中减少神经胶质瘤的生长

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The present study was undertaken to examine the effect of Fructus ligustri lucidi (FLL) extracts on glioma cell growth and to determine the underlying mechanism by which FLL extracts exert anticancer properties in human U87MG glioma cells. The FLL extracts resulted in cell death in a dose- and time-dependent manner. Western blot analysis showed that treatment with FLL extracts caused down-regulation of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway. Overexpression of Akt prevented the cell death induced by the FLL extracts. The FLL extracts caused a decrease in the expression of mammalian target of rapamycin (mTOR) and the FLL extract-induced cell death was increased by the mTOR inhibitor rapamycin. The FLL extracts decreased the expression of survivin. Oral administration of FLL extracts in subcutaneous U87MG xenograft models reduced the glioma tumor volume. These findings indicate that the FLL extracts resulted in glioma cell death through regulation of the Akt/mTOR/survivin pathway in vitro and inhibited glioma tumor growth in vivo. These data suggest that the FLL extracts may serve as a potential therapeutic agent for malignant human gliomas.
机译:进行本研究以检查大果枸杞提取物对神经胶质瘤细胞生长的影响,并确定其在人U87MG神经胶质瘤细胞中发挥抗癌作用的潜在机制。 FLL提取物以剂量和时间依赖性方式导致细胞死亡。蛋白质印迹分析表明,用FLL提取物进行处理会导致磷脂酰肌醇3激酶(PI3K)/ Akt通路的下调。 Akt的过度表达阻止了FLL提取物诱导的细胞死亡。 FLL提取物引起哺乳动物雷帕霉素靶标(mTOR)的表达降低,而mTOR抑制剂雷帕霉素使FLL提取物诱导的细胞死亡增加。 FLL提取物降低了survivin的表达。在皮下U87MG异种移植模型中口服FLL提取物可减少神经胶质瘤的体积。这些发现表明,FLL提取物通过体外调节Akt / mTOR / survivin途径导致神经胶质瘤细胞死亡,并在体内抑制神经胶质瘤的生长。这些数据表明,FLL提取物可作为人类恶性神经胶质瘤的潜在治疗剂。

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