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目的探讨灰树花β多糖在抗肿瘤细胞中的作用和协同化疗药物增加其杀伤肿瘤细胞的作用。另外通过对p53和M DM 2的研究,发现了两者协同作用的分子机理。方法用CCK-8方法测定了灰树花β多糖协同化疗药物处理HCT 116后的细胞存活率(cell surv iva l rate,CSR);用PCR的方法测定了p53、M DM 2基因的表达。结果(1)灰树花β多糖对肿瘤细胞的直接杀伤作用高于灵芝多糖。(2)灰树花β多糖协同化疗药物增强其对肿瘤细胞的杀伤作用。(3)灰树花β多糖协同化疗药物的分子机理和抑制抑癌基因p53的拮抗物M DM 2基因的表达相关。结论灰树花β多糖具有直接杀伤肿瘤作用和化学药物协同抗肿瘤作用。
Objective To explore the role of Grifola frondosa β-polysaccharide in anti-tumor cells and to increase its killing effect on tumor cells by chemotherapeutic drugs. In addition, through the research of p53 and M DM 2, we found out the molecular mechanism of their synergy. Methods Cell survivin rate (CSR) was determined by CCK-8 assay after treated with G-polysaccharide in combination with chemotherapeutic drug HCT 116. The expression of p53 and M DM 2 gene was determined by PCR. Results (1) The direct killing effect of Grifola frondosa polysaccharide on tumor cells was higher than that of Ganoderma lucidum polysaccharides. (2) Grifola frondosa polysaccharide synergistic chemotherapy drugs enhance its killing effect on tumor cells. (3) The molecular mechanism of synergistic chemotherapeutic drugs and the inhibition of the anti-oncogene p53 antagonist M DM 2 gene are related to the polysaccharide of Grifola frondosa. Conclusion Grifola frondosa polysaccharide has the direct killing effect on tumor and the synergistic anti-tumor effect of chemical drugs.