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目的研究羧甲基茯苓多糖对p388小鼠白血病的抗癌效果并探讨其治疗的分子机制。方法建立p388白血病动物模型、随机分组并给予治疗。采用流式细胞术、m R N A原位杂交和S蛳P法免疫细胞化学技术对小鼠外周血淋巴细胞的凋亡和bcl蛳2基因的m R N A和bcl蛳2蛋白进行检测。结果羧甲基茯苓多糖组(C M P)能使荷瘤小鼠生命延长35.88%,与化疗药物环磷酰胺(C TX)合用后可使小鼠的生存期延长70.05%。C M P组的生存期与模型组比较有统计学意义(P<0.05)。C M P可通过下调bcl蛳2基因诱导癌细胞凋亡,C M P与C TX合用后可显著下调bcl蛳2基因m R N A和蛋白的表达来诱导癌细胞凋亡(与C TX比较,P<0.05)。结论C M P有很好的抗白血病作用;C M P与C TX合用后可产生协同抗癌作用。
Objective To study the anticancer effect of carboxymethylhydrazine polysaccharide on p388 mouse leukemia and explore the molecular mechanism of its treatment. Methods A p388 leukemia animal model was established, randomized and treated. Flow cytometry, m R N A in situ hybridization and S蛳P immunocytochemistry were used to detect the apoptosis of peripheral blood lymphocytes in mice and m R N A and bcl蛳2 proteins of bcl蛳2 gene. Results The carboxymethyl guanosyl polysaccharide group (C M P) could prolong the life of tumor-bearing mice by 35.88%. Combined with the chemotherapy drug cyclophosphamide (C TX), the survival time of mice could be extended by 70.05%. The survival time of the C M P group was statistically significant compared with the model group (P < 0.05). C M P can induce apoptosis of cancer cells by down-regulating bcl蛳2 gene. Combined use of C M P and C TX can significantly down-regulate the expression of bcl蛳2 gene m R N A and protein to induce apoptosis of cancer cells (compared with C TX, P<0.05). Conclusion C M P has a good anti-leukemia effect; C M P and C TX can produce a synergistic anti-cancer effect.