白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2011年
1期
35-38
,共4页
江庭秀%顾伟英%邱国强%王志林%吴浩清%华晓莹%贺白%吴炜%谢晓宝%曹祥山
江庭秀%顧偉英%邱國彊%王誌林%吳浩清%華曉瑩%賀白%吳煒%謝曉寶%曹祥山
강정수%고위영%구국강%왕지림%오호청%화효형%하백%오위%사효보%조상산
肿瘤,实验性%辛伐他汀%K562细胞%细胞增殖%细胞凋亡
腫瘤,實驗性%辛伐他汀%K562細胞%細胞增殖%細胞凋亡
종류,실험성%신벌타정%K562세포%세포증식%세포조망
Neoplasms,experimental%Simvastatin%K562 cells%Cell proliferation%Apoptosis
目的 探讨辛伐他汀(SV)联合阿糖胞苷(Ara-C)对K562细胞增殖与凋亡的影响.方法 不同浓度SV和Ara-C单用或者联合处理K562细胞,对照组为K562细胞.药物作用24、48、72 h后收集细胞,分别观察各组细胞形态,采用MTT法检测不同组别细胞的生长抑制率,采用流式细胞术检测细胞早期凋亡率、细胞坏死比例.结果 SV联合Ara-C组与单药组相比细胞形态明显有核固缩现象,且可见凋亡小体形成,并且随着处理时间的增加,抑制率也增大.其中15 μmol/L SV联合20 μmol/LAra-C的细胞抑制作用最为显著,72 h细胞抑制率为(72±1)%,明显高于15 μmol/L SV组的(45±2)%和20μmol/LAra-C组的(44±0)%(P＜0.01),表现为协同抑制作用(24、48 h金氏Q值为1.24和1.19).流式细胞术检测发现20、15和10μmol/LSV组K562细胞早期凋亡率AnnexinV明显高于对照K562细胞(P＜0.01),而且随着时间延长和剂量的增大早期凋亡率也增加(P＜0.05).20和15 μmol/LSV组早期凋亡率均高于10 μmol/LSV组,而前两者之间差异无统计学意义(P＞0.05).晚期凋亡细胞率(PI)各组中差异均无统计学意义(P＞0.05).结论 SV体外抑制K562细胞增殖及诱导细胞凋亡,SV与Ara-C具有协同作用,增加了K562细胞对化疗药物的敏感性.15 μmol/L可能为SV体外最佳作用浓度.
目的 探討辛伐他汀(SV)聯閤阿糖胞苷(Ara-C)對K562細胞增殖與凋亡的影響.方法 不同濃度SV和Ara-C單用或者聯閤處理K562細胞,對照組為K562細胞.藥物作用24、48、72 h後收集細胞,分彆觀察各組細胞形態,採用MTT法檢測不同組彆細胞的生長抑製率,採用流式細胞術檢測細胞早期凋亡率、細胞壞死比例.結果 SV聯閤Ara-C組與單藥組相比細胞形態明顯有覈固縮現象,且可見凋亡小體形成,併且隨著處理時間的增加,抑製率也增大.其中15 μmol/L SV聯閤20 μmol/LAra-C的細胞抑製作用最為顯著,72 h細胞抑製率為(72±1)%,明顯高于15 μmol/L SV組的(45±2)%和20μmol/LAra-C組的(44±0)%(P＜0.01),錶現為協同抑製作用(24、48 h金氏Q值為1.24和1.19).流式細胞術檢測髮現20、15和10μmol/LSV組K562細胞早期凋亡率AnnexinV明顯高于對照K562細胞(P＜0.01),而且隨著時間延長和劑量的增大早期凋亡率也增加(P＜0.05).20和15 μmol/LSV組早期凋亡率均高于10 μmol/LSV組,而前兩者之間差異無統計學意義(P＞0.05).晚期凋亡細胞率(PI)各組中差異均無統計學意義(P＞0.05).結論 SV體外抑製K562細胞增殖及誘導細胞凋亡,SV與Ara-C具有協同作用,增加瞭K562細胞對化療藥物的敏感性.15 μmol/L可能為SV體外最佳作用濃度.
목적 탐토신벌타정(SV)연합아당포감(Ara-C)대K562세포증식여조망적영향.방법 불동농도SV화Ara-C단용혹자연합처리K562세포,대조조위K562세포.약물작용24、48、72 h후수집세포,분별관찰각조세포형태,채용MTT법검측불동조별세포적생장억제솔,채용류식세포술검측세포조기조망솔、세포배사비례.결과 SV연합Ara-C조여단약조상비세포형태명현유핵고축현상,차가견조망소체형성,병차수착처리시간적증가,억제솔야증대.기중15 μmol/L SV연합20 μmol/LAra-C적세포억제작용최위현저,72 h세포억제솔위(72±1)%,명현고우15 μmol/L SV조적(45±2)%화20μmol/LAra-C조적(44±0)%(P＜0.01),표현위협동억제작용(24、48 h금씨Q치위1.24화1.19).류식세포술검측발현20、15화10μmol/LSV조K562세포조기조망솔AnnexinV명현고우대조K562세포(P＜0.01),이차수착시간연장화제량적증대조기조망솔야증가(P＜0.05).20화15 μmol/LSV조조기조망솔균고우10 μmol/LSV조,이전량자지간차이무통계학의의(P＞0.05).만기조망세포솔(PI)각조중차이균무통계학의의(P＞0.05).결론 SV체외억제K562세포증식급유도세포조망,SV여Ara-C구유협동작용,증가료K562세포대화료약물적민감성.15 μmol/L가능위SV체외최가작용농도.
Objective To investigate the effect of simvastatin (SV) in combination with cytosine arabinoside (ARA-C) on the proliferation and apoptosis of K562 cells. Methods Human K562 cells were incubated with SV and cytosine arabinoside alone or in combination and K562 cells without any treatment were taken as normal control. Cells in different groups were collected at 24, 48 and 72 h after incubation for further detections. Morphological changes by Wright stain were performed. MTT method was used to assay the growth inhibition rate and cytoflowmetry was used to detect the early stage apoptosis ratio and cell necrosis ratio. Results Compared with Ara-C group and SV group, cells in the group treated with SV combined with Ara-C showed obvious karyopyknosis,apoptosis bodies formation and significant cell growth inhibition, which were positively correlated with culture time. Combination of 15 μmol/L SV and Ara-C showed the most significant cell growth inhibition with a inhibition rate of (72±1) % at 72 h of culture, as was significantly higher than that of 15 μmol/L SV group (45±2) % and 20 μmol/L Ara-C group (44±0) % (P ＜0.01),furthermore, combination of 15 μmol/L simvastatin and Ara-C showed synergistic inhibition with Q value of 1.24 and 1.19 at 24 h and 48 h in each. The apoptosis rates at early stage (AnnexinV) detected by flow cytometry in 20 μmol/L, 15 μmol/L and 10 μmol/L SV treated K562 cells were significantly higher than that in normal K562 cells (P ＜0.01), as were positively correlated with culture time and SV dose (P ＜0.05). There were no significant difference of early apoptosis rate between the 20 μmol/L SV and 15 μmol/L SV groups (P ＞0.05), yet the very two were both higher than that of 10 μmol/L SV group (P ＜0.05). There were no statistic differences of late apoptosis rate (PI) amongdifferent treated groups (P ＞0.05). Conclusion SV inhibited K562 cell proliferation and induced cell apoptosis in vitro, and combination of SV and Ara-C exhibited obvious synergistic inhibition and apoptosis, which may increase the sensitivity of K562 cell to chemotherapy. SV at 15 μmol/L may be the best concentration for K562 cells in vitro.
