CAJ | 학술논문

目的探讨冬凌草甲素体外诱导胃癌SGC-7901细胞凋亡和细胞周期阻滞的作用及其机制.方法 10～80 μmol/L冬凌草甲素分别处理SGC-7901细胞后,CCK8法检测冬凌草甲素体外对SGC-7901细胞抑制生长的作用;用流式细胞仪分别观察冬凌草甲素诱导凋亡及细胞周期阻滞.Western blot测定凋亡相关蛋白的表达.结果冬凌草甲素对SGC-7901细胞有明显的生长抑制作用,并随着药物浓度的增加(10～80 μmol/L)而逐渐增强,呈浓度、时间依赖关系.此外,流式细胞术检测发现,冬凌草甲素浓度为0、10、40、60、80 μmol/L,作用24 h后,G_2/M期细胞数分别是(9.90±1.17)%、(9.94±0.27)%、(11.76±0.16)%、(15.64±1.48)%和(22.59±1.01)%;而S期细胞比例分别为(31.79±1.03)%、(30.90±0.47)%、(29.25±0.80)%、(21.46±1.61)%、(18.81±0.61)%,冬凌草甲素能够使得SGC-7901细胞周期呈剂量依赖性阻滞于G_2/M期;冬凌草甲素浓度为80 μmol/L,作用12、24 h后,凋亡率分别为(12.78±1.54)%、(20.62±2.39)%,明显高于对照组的(9.92±0.56)%,其能使SGC-7901细胞发生凋亡.随着冬凌草甲素作用时间延长,SGC-7901细胞的bel-2蛋白表达逐渐减弱,前体Caapase-3被激活.结论冬凌草甲素能够诱导SGC-7901细胞产生凋亡,并使细胞周期阻滞在G_2/M期.其凋亡机制可能与下调bcl-2蛋白表达及Caspase-3的激活相关.
목적 탐토동릉초갑소체외유도위암SGC-7901세포조망화세포주기조체적작용급기궤제.방법 10～80 μmol/L동릉초갑소분별처리SGC-7901세포후,CCK8법검측동릉초갑소체외대SGC-7901세포억제생장적작용;용류식세포의분별관찰동릉초갑소유도조망급세포주기조체.Western blot측정조망상관단백적표체.결과 동릉초갑소대SGC-7901세포유명현적생장억제작용,병수착약물농도적증가(10～80 μmol/L)이축점증강,정농도、시간의뢰관계.차외,류식세포술검측발현,동릉초갑소농도위0、10、40、60、80 μmol/L,작용24 h후,G_2/M기세포수분별시(9.90±1.17)%、(9.94±0.27)%、(11.76±0.16)%、(15.64±1.48)%화(22.59±1.01)%;이S기세포비례분별위(31.79±1.03)%、(30.90±0.47)%、(29.25±0.80)%、(21.46±1.61)%、(18.81±0.61)%,동릉초갑소능구사득SGC-7901세포주기정제량의뢰성조체우G_2/M기;동릉초갑소농도위80 μmol/L,작용12、24 h후,조망솔분별위(12.78±1.54)%、(20.62±2.39)%,명현고우대조조적(9.92±0.56)%,기능사SGC-7901세포발생조망.수착동릉초갑소작용시간연장,SGC-7901세포적bel-2단백표체축점감약,전체Caapase-3피격활.결론 동릉초갑소능구유도SGC-7901세포산생조망,병사세포주기조체재G_2/M기.기조망궤제가능여하조bcl-2단백표체급Caspase-3적격활상관.
Objective To investigate the in vitro cell cycle arrest and apoptosis inducing effects of oridonin on SGC-7901 cell lines and the action mechanisms. Methods After administration of 10-80 μmol/L oridonin for 24-120 h, the CCK8 method was used to investigate the inhibitory effect of oridonin on SGC-7901 cells. Cell apoptosis and cell cycle arrest were investigated by flow cytometry (FCM). The ex-pression of apoptosis related proteins was detected using Western blotting. Results Oridonin could signifi-cantly inhibit the growth of SGC-7901 cells in both time-dependent and dose-dependent manners. FCM re-vealed that after treatment with different concentrations of ofidonin (0, 10, 40, 60, 80 μmol/L) for 24 h, the nnmber of G_2/M stage cells was (9.90±1.17)%, (9.94±0.27)%, (11.76±0. 16)%, (15.64± 1.48)%, (22.59 ± 1.01)%, and that of S stage cells was (31.79 ±1.03)%, (30.90±0.47)%, (29. 25 ± 0. 80 ) %, (21.46 ±1.61 ) %, (18. 81± 0.61 ) % respectively. The apoptotic rate was (9. 92± 0.56)%, (12.78±1.54)% and (20.62±2.39)% respectively within 0, 12 and 24 h after treatment with 80 μmol/L oridonin. With the extension of oridonin treatment, the bcl-2 protein expression in SGG-7901 cells was gradually reduced, and pro-caspase 3 was activated. Conclusion Oridonin can induce ap-optosis and G_2/M cell cycle arrest in SGC-7901 cells, which was probably contributed to the down-regula-tion of protein bcl-2 as well as activation of caspase-3.