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Polysaccharide-induced apoptosis in H22 cells through G2/M arrest and BCL2/BAX caspase-activated Fas pathway

机译:多糖通过G2 / M阻滞和BCL2 / BAX caspase激活的Fas途径诱导H22细胞凋亡

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The aim of the present work was to investigate the effect and the mechanism of growth inhibition on mouse H22 hepatocarcinoma cell of ascitic tumor induced by cartilage polysaccharides (PS). Our results showed that PS prolonged the survival time of the mice and increased the life span. In addition, PS induced the apoptosis of the H22 cells with the typical apoptotic morphological and biochemical changes confirmed by HE staining and TUNEL assay. The subsequent analysis of cell cycle distribution and relevant proteins revealed that decrease of cells in G0/G1phase and a G2/M arrest might due to the down-regulation of Cyclin D1 and AFP and up-regulation of P21 proteins. Moreover, BCL2/BAX caspase-activated Fas pathway was activated in PS-induced H22 apoptosis.
机译:本研究的目的是研究软骨多糖(PS)诱导的腹水对小鼠H22肝癌细胞的生长抑制作用及其机制。我们的结果表明PS延长了小鼠的存活时间并延长了寿命。此外,PS诱导了H22细胞的凋亡,并通过HE染色和TUNEL分析证实了典型的凋亡形态和生化变化。随后对细胞周期分布和相关蛋白的分析表明,G0 / G1期细胞减少和G2 / M停滞可能归因于细胞周期蛋白D1和AFP的下调以及P21蛋白的上调。此外,BCL2 / BAX caspase激活的Fas途径在PS诱导的H22细胞凋亡中被激活。

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