Objective: To investigated the anti-tumor in vivo effect and mechanism of the acid RNA protein complex (FA-2-b-β) of Agaricus blazei Murrill extract.
Methods: CCK-8 method was used to detected the inhibitory effect of FA-2-b-β on proliferation of primary CML cells from newly diagnosed CML patients, the CML mouse model was established by trail-venous injection of primary CML cells, and the survival time, blood cell count and body weight were observed, the immunoflouresence and immunehistochemistry analysis, RT-qPCR, Western bolt were used to detemine the expression of caspase-3 signal pathway-related apoptosis genes and proteins.
Results: The experiments in vitro showed that the proliferative inhibitory rate in drug-treated group increased with concentration- and time-dependent manner (r24=0.9092, r48=0.9442, r72=0.9546), the inter group comparison showed the statistical difference of results. The experiments in vitro showed that the survival time prolonged, blood cell count increased and body weight recovered in FA-2-b-β-treated group and imatinib-treated group, despite the WBC count is still high. The RT-qPCR and Western blot showed that the expression of BAX and caspase-3 gene and protein were up-regulated, the expression of BCL-2, cytochroime C, caspase-8, caspase-9 and BCL-ABL gene and protein were down-regulated.
Conclusion: The FA-2-b-β can induce apoptosis of primary CML cells and prolong the survival time of CML model mouse, which may be related with the caspase-3 signal pathway related genes and proteins.
题目: FA-2-b-β对慢性髓系白血病原代细胞的增殖抑制作用及其相关机制.
目的: 探讨秦巴硒菇提取物酸性RNA蛋白复合物(FA-2-b-β) 抗慢性髓系白血病的效果及机制。.
方法: 应用CCK-8法检测不同浓度FA-2-b-β对初诊慢性髓系白血病患者原代细胞增殖抑制作用;通过尾静脉注射原代白血病细胞建立慢性髓系白血病小鼠模型, 观察模型小鼠生存期、血细胞数、体重变化;采用免疫荧光、免疫组织化学法、RT-qPCR及Western blot 法检测caspase3信号通路相关凋亡基因和蛋白的表达。.
结果: 体外实验显示, 各药物浓度组中原代细胞增殖抑制率升高, 且呈浓度时间依赖性(r24=0.9082, r48=0.9442, r72=0.9546)。组间比较差异具有统计学意义。体内实验显示, 实验组(FA-2-b-β) 和阳性对照组(伊马替尼)模型小鼠生存期均延长, 并且血细胞数升高及体重恢复至正常, 尽管白细胞数仍高; BAX、Caspase-3基因和蛋白表达上调, BCL-2、Cytochrome C、 caspase 8、caspase 9、BCL/ABL基因和蛋白表达下降。.
结论: FA-2-b-β诱导慢性髓系白血病原代细胞凋亡, 可延长慢性髓系白血病模型小鼠的生存期, 其机制可能与caspase-3信号通路相关凋亡基因和蛋白有关。.