CAJ | 학술논문

在相同条件下，通过测定细胞死亡率、DNA电泳、末端脱氧核苷转移酶介导的生物素标记寡核苷酸末端标记（TUNEL），对比观察足叶已甙（VP-16）作用下人胃低分化腺癌细胞（BGS-180 ）和慢性淋巴细胞性白血病细胞（HL-60）的凋亡情况。结果显示，低剂量VP-16短时间作用HL-60细胞，细胞的死亡以凋亡为主，并可被蛋白激酶C（PKC）激活所抑制；而VP-16致BGS-180 细胞的死亡以坏死为主，不被PKC所抑制。细胞外Ca2+螯合剂EDTA对VP-16作用下两种细胞的死亡无影响。提示化疗药对HL-60细胞和BGS-180细胞的作用机制不同，在其导致BGS-180细胞的死亡中凋亡并不是主要的方式。
재상동조건하，통과측정세포사망솔、DNA전영、말단탈양핵감전이매개도적생물소표기과핵감산말단표기（TUNEL），대비관찰족협이대（VP-16）작용하인위저분화선암세포（BGS-180 ）화만성림파세포성백혈병세포（HL-60）적조망정황。결과현시，저제량VP-16단시간작용HL-60세포，세포적사망이조망위주，병가피단백격매C（PKC）격활소억제；이VP-16치BGS-180 세포적사망이배사위주，불피PKC소억제。세포외Ca2+오합제EDTA대VP-16작용하량충세포적사망무영향。제시화료약대HL-60세포화BGS-180세포적작용궤제불동，재기도치BGS-180세포적사망중조망병불시주요적방식。
Programmed cell death(PCD)of human leukemic HL-60 cell and human poorly differentiated gastric adenocarcinoma cell BGS-180 induced by efoposid(VP-16) was preliminarily observed comparatively in the same experimental condition through rate of cell death, DNA agarose gels electrophoresis and terminal deoxynucleotidyl transferase(TdT) mediated biotin-11-dUTP nickend labeling(TUNEL).It was found that apoptosis is the main pattern of HL-60 cell death induced by low does VP-16 in a short time, and it can be suppressed when protein kinase C(PKC) is activated. The main pattern of BGS-180 cell death induced by VP-16 is necrosis, and PCK activation does not affect its necrosis rate. Extracellular Ca2+ reduction do not affect BGS-180 and HL-60 cell death rate. The mechanism of VP-16 action on BGS-180 and HL-60 cell is different, apoptosis is not the main pattern of cell BGS-180 death induced by VP-16.