大连医科大学学报
大連醫科大學學報
대련의과대학학보
JOURNAL OF DALIAN MEDICAL UNIVERSITY
2014年
1期
18-22
,共5页
易翠林%时京杰%包雪%王玉林
易翠林%時京傑%包雪%王玉林
역취림%시경걸%포설%왕옥림
细胞毒%肿瘤多药耐药%细胞周期%线粒体膜电位%细胞凋亡
細胞毒%腫瘤多藥耐藥%細胞週期%線粒體膜電位%細胞凋亡
세포독%종류다약내약%세포주기%선립체막전위%세포조망
SRB%cytotoxicity%cell life-cycle%mitochondria membrane potential%apoptosis
目的:系统评价KA2012 MBL复合提取液的抗肿瘤活性及对P-gp介导的肿瘤多药耐药的克服能力,并初步探讨KA2012 MBL复合提取液的抗肿瘤机制。方法应用SRB法测定KA2012 MBL复合提取液对K562/A、K562/S和HGC-27的细胞毒活性,应用流式细胞术检测KA2012 MBL复合提取液对K562/S细胞的细胞周期阻滞作用、凋亡诱导作用和对其线粒体膜电位的影响作用。结果 KA2012 MBL复合提取液对肿瘤细胞株K562/A、K562/S和HGC-27均具有细胞毒活性,IC50值分别为(1.12±0.15)%(v/v%)、(1.18±0.04)%(v/v%)、(1.21±0.17)%(v/v%),并可有效克服P-gp介导的肿瘤多药耐药。流式细胞术检测结果显示KA2012MBL复合提取液可有效降低K562/S细胞的线粒体膜电位,并可使 K562/S 细胞阻滞在 G0/G1期,从而诱导其凋亡。结论KA2012 MBL复合提取液通过诱导肿瘤细胞凋亡而杀死肿瘤细胞,同时能克服P-gp介导的肿瘤多药耐药。
目的:繫統評價KA2012 MBL複閤提取液的抗腫瘤活性及對P-gp介導的腫瘤多藥耐藥的剋服能力,併初步探討KA2012 MBL複閤提取液的抗腫瘤機製。方法應用SRB法測定KA2012 MBL複閤提取液對K562/A、K562/S和HGC-27的細胞毒活性,應用流式細胞術檢測KA2012 MBL複閤提取液對K562/S細胞的細胞週期阻滯作用、凋亡誘導作用和對其線粒體膜電位的影響作用。結果 KA2012 MBL複閤提取液對腫瘤細胞株K562/A、K562/S和HGC-27均具有細胞毒活性,IC50值分彆為(1.12±0.15)%(v/v%)、(1.18±0.04)%(v/v%)、(1.21±0.17)%(v/v%),併可有效剋服P-gp介導的腫瘤多藥耐藥。流式細胞術檢測結果顯示KA2012MBL複閤提取液可有效降低K562/S細胞的線粒體膜電位,併可使 K562/S 細胞阻滯在 G0/G1期,從而誘導其凋亡。結論KA2012 MBL複閤提取液通過誘導腫瘤細胞凋亡而殺死腫瘤細胞,同時能剋服P-gp介導的腫瘤多藥耐藥。
목적:계통평개KA2012 MBL복합제취액적항종류활성급대P-gp개도적종류다약내약적극복능력,병초보탐토KA2012 MBL복합제취액적항종류궤제。방법응용SRB법측정KA2012 MBL복합제취액대K562/A、K562/S화HGC-27적세포독활성,응용류식세포술검측KA2012 MBL복합제취액대K562/S세포적세포주기조체작용、조망유도작용화대기선립체막전위적영향작용。결과 KA2012 MBL복합제취액대종류세포주K562/A、K562/S화HGC-27균구유세포독활성,IC50치분별위(1.12±0.15)%(v/v%)、(1.18±0.04)%(v/v%)、(1.21±0.17)%(v/v%),병가유효극복P-gp개도적종류다약내약。류식세포술검측결과현시KA2012MBL복합제취액가유효강저K562/S세포적선립체막전위,병가사 K562/S 세포조체재 G0/G1기,종이유도기조망。결론KA2012 MBL복합제취액통과유도종류세포조망이살사종류세포,동시능극복P-gp개도적종류다약내약。
Objective To evaluate the antitumor activity of KA 2012 MBL and the ability to overcome P -gp mediated MDR in vitro.Methods The cytotoxicity of KA2012MBL against K562/A, K562/S and HGC-27 were determined by SRB as-say.FACS analysis was used to detect the cell cycle arrest activity and apoptosis induction activity of KA 2012MBL on K562/S cells and the loss of mitochondria membrane potential (MMP) of K562/S cells caused by KA2012MBL.Results KA2012MBL showed excellent in vitro cytotoxicity against K562/A,K562/S and HGC-27, with IC50 of (1.12 ±0.15)%(v/v%),(1.18 ±0.04)%(v/v%) and (1.21 ±0.17)%(v/v%),respectively.It also shows ability to overcome P -gp mediated MDR.Furthermore, KA2012MBL caused the loss of MMP of K562/S cells and cell cycle arrest at G 0/G1 phase, and induced the apoptosis of K562/S cells.Conclusion KA2012MBL exerts its antitumor activity by apoptosis induction in tumor cells, which indicates KA2012MBL would show very potent in vivo antitumor activity .Furthermore, KA2012MBL could overcome P-gp mediated MDR successfully .