中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
10期
2388-2391
,共4页
苌静%孙康%盛霞%秦建民
萇靜%孫康%盛霞%秦建民
장정%손강%성하%진건민
蟾毒灵%癌,肝细胞%增殖%凋亡
蟾毒靈%癌,肝細胞%增殖%凋亡
섬독령%암,간세포%증식%조망
Bufalin%Cancer,liver cell%Proliferation%Apoptosis
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.
目的 觀察蟾毒靈抗高轉移潛能肝癌細胞增殖凋亡作用.方法 體外培養人高轉移潛能HCC-LM3肝癌細胞,分彆加入不同濃度蟾毒靈(0.02、0.04、0.08 mg/L)和5-氟尿嘧啶(5-Fu,1.05、12.34、25.79 mg/L)作用肝癌細胞24、48、72 h後,採用細胞計數試劑盒(CCK-8)、流式細胞技術測定肝癌細胞生長、增殖週期變化和細胞凋亡.結果 同一時間點隨蟾毒靈濃度增加對肝癌細胞生長抑製率逐漸增加(F=14.823、15.623、4.737,P＜0.05),同一濃度隨作用時間延長蟾毒靈對肝癌細胞生長抑製率逐漸增加(F =44.757、43.256、19.682、17.112、50.765、31.214,P＜0.05).與對照組相比,蟾毒靈濃度增加導緻G1期肝癌細胞比例逐漸降低[IC50組:(43.96±3.52)％比(70.19 ±4.70)％ ,IC70組:(40.99±5.72)％比(70.19 ±4.70)％,F=23.924,P＜0.05],G2+S期肝癌細胞比例逐漸增加[IC50組:(56.04±3.52)％比(29.81±4.70)％,IC70組:(59.01±5.72)％比(29.81±4.70)％,F =23.924,P＜0.05].不同作用時間隨蟾毒靈濃度增加,肝癌細胞凋亡率逐漸增加(F=6.817、46.639、77.658,P＜0.05),且作用48 h[IC50組:(34.01±4.62)％比(22.02±1.29)％,IC70組:(47.60±4.41)％比(31.90±4.95)％,t=-6.381,P＜0.05]和72 h蟾毒靈誘導肝癌細胞凋亡率高于5-FU[IC50組:(52.01±6.63)％比(32.65±3.69)％,IC70組:(74.31±6.18)％比(47.85±4.52)％,t=-5.729,P＜0.05].結論 蟾毒靈通過阻滯肝癌細胞增殖于S期和G2期誘導細胞凋亡.
목적 관찰섬독령항고전이잠능간암세포증식조망작용.방법 체외배양인고전이잠능HCC-LM3간암세포,분별가입불동농도섬독령(0.02、0.04、0.08 mg/L)화5-불뇨밀정(5-Fu,1.05、12.34、25.79 mg/L)작용간암세포24、48、72 h후,채용세포계수시제합(CCK-8)、류식세포기술측정간암세포생장、증식주기변화화세포조망.결과 동일시간점수섬독령농도증가대간암세포생장억제솔축점증가(F=14.823、15.623、4.737,P＜0.05),동일농도수작용시간연장섬독령대간암세포생장억제솔축점증가(F =44.757、43.256、19.682、17.112、50.765、31.214,P＜0.05).여대조조상비,섬독령농도증가도치G1기간암세포비례축점강저[IC50조:(43.96±3.52)％비(70.19 ±4.70)％ ,IC70조:(40.99±5.72)％비(70.19 ±4.70)％,F=23.924,P＜0.05],G2+S기간암세포비례축점증가[IC50조:(56.04±3.52)％비(29.81±4.70)％,IC70조:(59.01±5.72)％비(29.81±4.70)％,F =23.924,P＜0.05].불동작용시간수섬독령농도증가,간암세포조망솔축점증가(F=6.817、46.639、77.658,P＜0.05),차작용48 h[IC50조:(34.01±4.62)％비(22.02±1.29)％,IC70조:(47.60±4.41)％비(31.90±4.95)％,t=-6.381,P＜0.05]화72 h섬독령유도간암세포조망솔고우5-FU[IC50조:(52.01±6.63)％비(32.65±3.69)％,IC70조:(74.31±6.18)％비(47.85±4.52)％,t=-5.729,P＜0.05].결론 섬독령통과조체간암세포증식우S기화G2기유도세포조망.
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.
