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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株K562凋亡和细胞周期的影响及其分子机制的研究

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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)-κB 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-κB/cyclin D1 signaling pathway serves a crucial role in cell cycle arrest and apoptosis of K562 cells.
机译:人参多糖(GPS)是葡萄糖和从人参提取的主要成分的聚合物,已被证明具有多种药理特性,包括抗肿瘤特性。为了进一步了解GPS的抗肿瘤功能,本研究旨在研究GPS对人白血病细胞K562细胞凋亡和细胞周期的影响及其潜在机制。结果表明,GPS可以在体外以浓度和时间依赖性的方式抑制K562细胞的增殖并诱导其凋亡。与对照组相比,GPS治疗后P38和c-Jun NH2末端激酶(JNK)mRNA的转录显着增加,而细胞外信号调节激酶(ERK)mRNA的转录显着减少(所有P <0.05 )。此外,GPS免疫显着抑制了磷酸化(p)-ERK,核因子(NF)-κBp65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,这通过免疫荧光和蛋白质印迹分析。总之,结果表明,GPS介导的MAPK /NF-κB/ cyclin D1信号通路在K562细胞的细胞周期阻滞和凋亡中起着至关重要的作用。

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