摘要
目的:探讨二氢杨梅素(AMP)联合细胞化疗药物丝裂霉素(MMC)对胃癌细胞SGC-7901的抑制作用。方法:体外培养人胃癌细胞株SGC-7901,分别设空白对照组、AMP组、MMC组以及AMP+MMC组。用MTT法观察细胞生长;流式细胞术分析细胞凋亡率;Western blotting检测细胞Bcl-2及survivin的表达情况。结果:在AMP组中,当浓度在2.2 mg/L-14.84 mg/L时,AMP对胃癌细胞生长均有抑制作用,以14.84 mg/L抑制作用最明显(60.85%±1.13%,P<0.05)。MMC随着浓度由1×10-3g/L增加至1×10g/L,其抑制率也由17.40%±0.30%增加至72.23%±1.36%,呈递增趋势。AMP联合MMC的抑制作用随着MMC浓度由1×10-3g/L增加至5×10-3g/L,抑制率也由21.83%±2.50%增加至46.70%±1.45%。联合治疗组优于单独给药组。AMP、MMC及AMP+MMC均可以下调Bcl-2及survivin的表达,其中AMP+MMC组下调作用最明显。结论:AMP联合MMC可以增强对胃癌细胞的抑制作用,联合应用可以减低MMC的剂量;其抑制肿瘤作用可能与下调Bcl-2及survivin蛋白的表达有关。
AIM： To investigate the synergistic effects of ampelopsin（AMP） and a chemotherapeutic drug mitomycin（MMC） on the proliferation of gastric cancer cell line SGC-7901.METHODS： SGC-7901 cells were cultured in vitro and divided into 4 groups： control group,AMP group,MMC group and AMP＋MMC group.Cell proliferation was measured by MTT method.The apoptotic index was examined by flow cytometry.The expression of apoptotic proteins,Bcl-2 and survivin,was detected by Western blotting.RESULTS： AMP at the concentrations ranging from 2.2 mg/L to 14.84 mg/L exerted inhibitory effect on the growth of SGC-7901 cells.Cell proliferation in AMP（14.84 mg/L） group was inhibitory by（60.85±1.13） %,significantly higher than that in control group（P0.05）.The inhibitory rates of cell proliferation varied from（17.40±0.30） % to（72.23±1.36） % when the concentrations of MMC increased from 1×10-3 g/L to 1×10-2 g/L.AMP combined with MMC showed a synergistic effect on the growth of SGC-7901 cells.The inhibitory rates of cell proliferation varied from（21.83±2.50） % to（46.70±1.45） % when the concentrations of MMC increased from 1×10-3g/L to 5×10-3g/L.The inhibitory effect of AMP plus MMC was higher than that of MMC or AMP alone.The protein levels of Bcl-2 and survivin were inhibited in AMP group,MMC group and AMP＋MMC group,and were significantly lower in AMP＋MMC group than those in AMP group or MMC group.CONCLUSION： AMP enhances the inhibitory effect of MMC on the growth of SGC-7901 cells.The mechanism is related to the inhibition of apoptotic protein expression.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2011年第7期1424-1427,共4页
Chinese Journal of Pathophysiology
