蟾毒灵抗高转移潜能肝癌细胞增殖凋亡的研究
Experimental study of bufalin on inhibiting cell proliferation and apoptosis in liver cancer cells with high metastatic potential
目的 观察蟾毒灵抗高转移潜能肝癌细胞增殖凋亡作用.方法 体外培养人高转移潜能HCC-LM3肝癌细胞,分别加入不同浓度蟾毒灵(0.02、0.04、0.08 mg/L)和5-氟尿嘧啶(5-Fu,1.05、12.34、25.79 mg/L)作用肝癌细胞24、48、72 h后,采用细胞计数试剂盒(CCK-8)、流式细胞技术测定肝癌细胞生长、增殖周期变化和细胞凋亡.结果 同一时间点随蟾毒灵浓度增加对肝癌细胞生长抑制率逐渐增加(F=14.823、15.623、4.737,P<0.05),同一浓度随作用时间延长蟾毒灵对肝癌细胞生长抑制率逐渐增加(F =44.757、43.256、19.682、17.112、50.765、31.214,P<0.05).与对照组相比,蟾毒灵浓度增加导致G1期肝癌细胞比例逐渐降低[IC50组:(43.96±3.52)%比(70.19 ±4.70)% ,IC70组:(40.99±5.72)%比(70.19 ±4.70)%,F=23.924,P<0.05],G2+S期肝癌细胞比例逐渐增加[IC50组:(56.04±3.52)%比(29.81±4.70)%,IC70组:(59.01±5.72)%比(29.81±4.70)%,F =23.924,P<0.05].不同作用时间随蟾毒灵浓度增加,肝癌细胞凋亡率逐渐增加(F=6.817、46.639、77.658,P<0.05),且作用48 h[IC50组:(34.01±4.62)%比(22.02±1.29)%,IC70组:(47.60±4.41)%比(31.90±4.95)%,t=-6.381,P<0.05]和72 h蟾毒灵诱导肝癌细胞凋亡率高于5-FU[IC50组:(52.01±6.63)%比(32.65±3.69)%,IC70组:(74.31±6.18)%比(47.85±4.52)%,t=-5.729,P<0.05].结论 蟾毒灵通过阻滞肝癌细胞增殖于S期和G2期诱导细胞凋亡.
更多Objective To investigate the inhibitory effectof Bufalin on human hepatocellulacarcinomcellwith high metastatipotential.MethodThe human hepatomcellwith high metastatipotential (HCC-LM3) were cultured in vitro.The bufalin warespectively added into culture fluid with variouconcentration of 0.02, 0.04, 0.08 mg/L.The 5-fluorouracil (5-Fu) warespectively added into culture fluid with variouconcentration of 1.05, 12.34, 25.79 mg/L.The cell growth, proliferative cycle and apoptosiwere respectively determined by cell counting kit-8 (CCK-8) assay and flow cytometry technique a24, 48, 72 h.ResultThe growth inhibitory rate of HCC-LM3 cellgradually increased with the increase of bufalin concentration athe same time (F =14.823, 15.623, 4.737, P < 0.05) owith the time extension of bufalin athe same concentration (F =44.757, 43.256, 19.682, 17.112,50.765, 31.214, P < 0.05).Compared with control group, the cell percentage of HCC-LM3 cellaG1 phase gradually decreased with the increase of bufalin concentration[IC50 : (43.96 ± 3.52) % vs.(70.19 ± 4.70) %, IC70 : (40.99 ± 5.72) % vs.(70.19-± 4.70) %, F =23.924, P < 0.05], and the cell percentage of HCC-LM3 cellaG2 pluphasegradually increased with the increase of bufalin concentration [IC50:(56.04±3.52)% vs.(29.81 ±4.70)%,IC70:(59.01 ±5.72)% vs.(29.81 ±4.70)%,F=23.924, P < 0.05].The apoptotirate of HCC-LM3 cellgradually increased with the increase of bufalin concentration avarioutime (F =6.817, 46.639, 77.658, P < 0.05).The apoptotirate of HCC-LM3 cellinduced by bufalin wahighethan thaof 5-Fu a48 h and 72 h [IC50 : (34.01 ± 4.62) % vs.(22.02 ±1.29)%,IC70:(47.60±4.41)% vs.(31.90 ±4.95)%,t=-6.381,P<0.05] and 72 h [IC50:(52.01±6.63)% vs.(32.65 ±3.69)%,IC70:(74.31 ±6.18)% vs.(47.85 ±4.52)%,=-5.729,P < 0.05].Conclusion Iione of the importanmechanismof bufalin in inhibiting the growth of human hepatocellulacarcinomcellwith high metastatipotential by blocking the cell proliferation aG2 pluphaseand inducing the cell apoptosis.
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