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目的观察人参皂苷Ro对小鼠胃癌MFC细胞增殖和凋亡的影响。方法给药组给予人参皂苷Ro,使其达到不同的终质量浓度(96,48,24,12,6μg/m L),作用于MFC细胞48h后,采用MTT染色法检测MFC细胞的增殖抑制率;用流式细胞仪检测MFC细胞周期和凋亡情况;建立MFC移植瘤小鼠模型,随机分为模型组(生理盐水),环磷酰胺(20 mg/kg)组和人参皂苷Ro(800,400,200 mg/kg)剂量组,连续灌胃给药10 d,处死小鼠,剥取瘤组织称量并计算抑瘤率。结果与6.0μg/m L组比较,人参皂苷Ro在12~96μg/m L范围内对MFC细胞的增殖的抑制率随浓度的增加而显著升高(P<0.01)。与空白对照组比较,人参皂苷Ro高剂量组的MFC细胞G0/G1期和凋亡率明显升高(P<0.01),G2/M期,S期明显降低(P<0.01)。人参皂苷Ro各剂量组均能显著抑制肿瘤生长,与模型组比较,各给药组肿瘤的质量明显降低(P<0.05),其中人参皂苷Ro高剂量组的抑瘤率62.7%。结论人参皂苷Ro对MFC移植瘤小鼠具有抑瘤作用,可能与诱导MFC细胞凋亡和抑制增殖有关。
Objective To observe the effect of ginsenoside Ro on the proliferation and apoptosis of mouse gastric cancer cell line MFC. Methods Ginsenoside Ro was administered to the treatment group to achieve different final concentrations (96, 48, 24, 12 and 6 μg / mL). After treated with MFC for 48 hours, the proliferation inhibition rate of MFC cells was measured by MTT assay The cell cycle and apoptosis of MFC were detected by flow cytometry. The mouse model of MFC xenografts was established and randomly divided into model group (normal saline), cyclophosphamide (20 mg / kg) group and ginsenoside Ro (800, 400, 200 mg / kg) dose group, continuous gavage administration for 10 days, mice were killed, stripped of tumor tissue weighed and calculated tumor inhibition rate. Results Compared with the 6.0μg / ml group, the inhibitory rate of Ginsenoside Ro in the range of 12 ~ 96μg / ml on the proliferation of MFC cells was significantly increased with the increase of concentration (P <0.01). Compared with the blank control group, G0 / G1 phase and apoptosis rate of MFC cells in high dose Ginsenoside Ro group were significantly increased (P <0.01), G2 / M phase and S phase were significantly decreased (P <0.01). The ginsenoside Ro dose groups were significantly inhibited tumor growth, compared with the model group, the quality of the tumor was significantly reduced (P <0.05), of which ginsenoside Ro high dose group of tumor inhibition rate of 62.7%. Conclusion Ginsenoside Ro has anti-tumor effect on MFC xenografts in mice, which may be related to the induction of apoptosis and the inhibition of proliferation in MFC cells.