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Research on the effect of ginseng polysaccharide on apoptosis and cell cycle of human leukemia cell line K562 and its molecular mechanisms

机译:人参多糖对人白血病细胞系K562细胞凋亡及细胞周期的影响及其分子机制

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摘要

Ginseng polysaccharide (GPS), a polymer of glucose and the primary constituent extracted from panax ginseng, has been documented to exert various pharmacological properties, including anti-tumor properties. To provide further insights into the anti-tumor functions of GPS, the present study was designed to investigate the effect of GPS on apoptosis and the cell cycle of human leukemia cell line K562 cells, and its underlying mechanisms. The results demonstrated that GPS could inhibit K562 cell proliferation and induce apoptosis in vitro in a concentration-and time-dependent manner. The transcription of P38 and c-Jun NH2-terminal kinase (JNK) mRNA were significantly augmented, while the transcription of extracellular signal-regulated kinase (ERK) mRNA were significantly reduced following treatment with GPS compared with the control group (all P < 0.05). In addition, GPS treatment markedly suppressed the expression of phosphorylated (p)-ERK, nuclear factor (NF)-kappa B p65 and cyclin D1, and increased the synthesis of p-P38 and p-JNK protein expression, as evidenced by immunofluorescence and western blotting analyses. In conclusion, the results indicate that the GPS-mediated MAPK/NF-kappa B/cyclin D1 signaling pathway serves a crucial role in cell cycle arrest and apoptosis of K562 cells.
机译:已经记录了人参多糖(GPS),葡萄糖聚合物和从Panax人参中提取的主要成分,以施加各种药理学性质,包括抗肿瘤性质。为了提供进一步了解GPS的抗肿瘤功能,本研究旨在探讨GPS对人白血病细胞系K562细胞细胞凋亡和细胞周期的影响及其潜在机制。结果表明,GPS可以抑制K562细胞增殖并以浓度和时间依赖的方式体外诱导细胞凋亡。 P38和C-JUM NH2-末端激酶(JNK)mRNA的转录显着增强,而细胞外信号调节激酶(ERK)mRNA的转录与对照组相比,GPS治疗明显减少(所有P <0.05 )。此外,GPS处理显着抑制了磷酸化(P) - 核,核因子(NF)-Kappa B P65和细胞周期蛋白D1的表达,并增加了P-P38和P-JNK蛋白表达的合成,如免疫荧光和所证明的Western Blotting分析。总之,结果表明,GPS介导的MAPK / NF-Kappa B / Cyclin D1信号传导途径在细胞周期停滞和K562细胞的凋亡中用于Cell循环滞留和凋亡的关键作用。

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