临床肿瘤学杂志
臨床腫瘤學雜誌
림상종류학잡지
CHINESE CLINICAL ONCOLOGY
2014年
7期
589-593
,共5页
Schisandrin B%卵巢癌%增殖%凋亡%Wnt/β-catenin信号通路
Schisandrin B%卵巢癌%增殖%凋亡%Wnt/β-catenin信號通路
Schisandrin B%란소암%증식%조망%Wnt/β-catenin신호통로
Schisandrin B%Human ovarian cancer%Proliferation%Apoptosis%Wnt/β-catenin signaling pathway
目的：探讨五味子乙素（ Sch B）对人卵巢癌Skov3细胞株的增殖、凋亡及Wnt/β-catenin信号通路的影响。方法采用0、1?0、10?0、20?0、50?0μmol/L Sch B处理Skov3细胞，采用四甲基偶氮唑盐（ MTT）法检测各浓度处理24、48、72和96h的增殖抑制率，Annexin-FITC/PI双染法检测不同浓度处理48h后的细胞凋亡情况，流式细胞仪检测各浓度处理48h后的细胞周期分布情况，Western blotting检测各浓度处理48h后细胞核Wnt/β-catenin信号通路中β-连接素（β-catenin）及下游靶分子C-myc、细胞周期素D1（ Cyclin D1）的蛋白水平，同时于各浓度处理48h后检测细胞质和细胞核的糖原合成酶激酶-3β（ GSK-3β）活性。结果 Sch B可呈剂量和时间依赖方式增加细胞增殖抑制率（ P＜0?05），作用48h后可呈剂量依赖方式升高早、晚期凋亡率及细胞质/胞核 GSK-3β活性（ P＜0?05）；除1?0μmol/L外，其余浓度作用48h 的 G0/G1期细胞比例均高于0μmol/L，S 期、G2/M 期细胞比例及β-catenin、C-myc 和 Cyclin D1蛋白水平均低于0μmol/L （ P＜0?05），且10?0、20?0、50?0μmol/L Sch B间的差异有统计学意义（ P＜0?05）。结论 Sch B可以抑制Skov3细胞株的增殖并促进其凋亡和细胞周期阻滞，以及抑制Wnt/β-catenin通路的激活。
目的：探討五味子乙素（ Sch B）對人卵巢癌Skov3細胞株的增殖、凋亡及Wnt/β-catenin信號通路的影響。方法採用0、1?0、10?0、20?0、50?0μmol/L Sch B處理Skov3細胞，採用四甲基偶氮唑鹽（ MTT）法檢測各濃度處理24、48、72和96h的增殖抑製率，Annexin-FITC/PI雙染法檢測不同濃度處理48h後的細胞凋亡情況，流式細胞儀檢測各濃度處理48h後的細胞週期分佈情況，Western blotting檢測各濃度處理48h後細胞覈Wnt/β-catenin信號通路中β-連接素（β-catenin）及下遊靶分子C-myc、細胞週期素D1（ Cyclin D1）的蛋白水平，同時于各濃度處理48h後檢測細胞質和細胞覈的糖原閤成酶激酶-3β（ GSK-3β）活性。結果 Sch B可呈劑量和時間依賴方式增加細胞增殖抑製率（ P＜0?05），作用48h後可呈劑量依賴方式升高早、晚期凋亡率及細胞質/胞覈 GSK-3β活性（ P＜0?05）；除1?0μmol/L外，其餘濃度作用48h 的 G0/G1期細胞比例均高于0μmol/L，S 期、G2/M 期細胞比例及β-catenin、C-myc 和 Cyclin D1蛋白水平均低于0μmol/L （ P＜0?05），且10?0、20?0、50?0μmol/L Sch B間的差異有統計學意義（ P＜0?05）。結論 Sch B可以抑製Skov3細胞株的增殖併促進其凋亡和細胞週期阻滯，以及抑製Wnt/β-catenin通路的激活。
목적：탐토오미자을소（ Sch B）대인란소암Skov3세포주적증식、조망급Wnt/β-catenin신호통로적영향。방법채용0、1?0、10?0、20?0、50?0μmol/L Sch B처리Skov3세포，채용사갑기우담서염（ MTT）법검측각농도처리24、48、72화96h적증식억제솔，Annexin-FITC/PI쌍염법검측불동농도처리48h후적세포조망정황，류식세포의검측각농도처리48h후적세포주기분포정황，Western blotting검측각농도처리48h후세포핵Wnt/β-catenin신호통로중β-련접소（β-catenin）급하유파분자C-myc、세포주기소D1（ Cyclin D1）적단백수평，동시우각농도처리48h후검측세포질화세포핵적당원합성매격매-3β（ GSK-3β）활성。결과 Sch B가정제량화시간의뢰방식증가세포증식억제솔（ P＜0?05），작용48h후가정제량의뢰방식승고조、만기조망솔급세포질/포핵 GSK-3β활성（ P＜0?05）；제1?0μmol/L외，기여농도작용48h 적 G0/G1기세포비례균고우0μmol/L，S 기、G2/M 기세포비례급β-catenin、C-myc 화 Cyclin D1단백수평균저우0μmol/L （ P＜0?05），차10?0、20?0、50?0μmol/L Sch B간적차이유통계학의의（ P＜0?05）。결론 Sch B가이억제Skov3세포주적증식병촉진기조망화세포주기조체，이급억제Wnt/β-catenin통로적격활。
Objective To explore the influences of Schisandrin B ( Sch B) on proliferation, apoptosis and Wnt/β-catenin signaling pathway of SKOV3 human ovarian cancer cells. Methods The SKOV3 cells were treated with different concentrations of Sch B ( 0, 1?0, 10?0, 20?0, 50?0μmol/L) . The MTT was used to measure the proliferation inhibition rates at 24, 48, 72 and 96h treated with different concentrations of Sch B. The Annexin-FITC/PI double staining was employed to detect cell apoptosis at 48h after treat-ment with different concentrations of Sch B. The cycle distribution at 48h after treatment with Sch B was detected by flow cytometry. The Western blotting was used to measure the nuclearβ-catenin protein levels in Wnt/β-catenin signaling pathway as well as its downstream target C-myc and cyclin D1. The cytoplasm/nucleus activities of glycogen synthase kinase 3β ( GSK-3β) at 48h after treatment with different concentrations of Sch B were measured by activity assay kit. Results The Sch B can increase the proliferation inhibition rates in a dose-and time-dependent manner, and elevate the early and late apoptosis and cytoplasm/nucleus activities of GSK-3βat 48h after treatment. In addition to 1?0μmol/L, the proportion of cells in G0/G1 phase of the remaining concentrations were higher than those of 0μmo/L ( P<0?05) , and the proportion of cells in S phase and G2/M phase andβ-catenin, C-myc and Cyclin D1 protein levels were lower than those of 0μmo/L ( P<0?05) . Conclusion Sch B can inhibit the proliferation, promote apoptosis and cell cycle arrest and inhibit the activation of Wnt/β-catenin pathway.
