CAJ | 학술논문

目的探讨旋覆花内酯(ABL)-N诱导前列腺癌细胞凋亡的作用及其机制.方法 0～40μmol/L ABL-N分别处理前列腺痛细胞后,利用噻唑蓝(MTF)检测对细胞增长的抑制作用;流式细胞学、TUNEL染色等方法检测其诱导凋亡的作用,并检测Capase活性,Western blot测定bax、bel-2水平变化.结果 ABL-N明显抑制前列腺癌细胞PC3、LNCaP及DU145的生长,并呈剂量依赖性.40 μmol/L ABL-N作用24 h后,(73.34±4.41)%的PrEC细胞存活,而3种前列腺癌细胞分别为(11.92±2.31)%、(12.55±1.94)%、(13.28±2.26)%.膜联蛋白/碘化丙锭(Annexin V/PI)及TUNEL染色表明ABL-N呈剂量依赖性诱导PC3凋亡.ABL-N可激活Caspase活性,尤其Caspase-3,20μmol/L ABL-N作用24 h后其活性是对照组的4.23倍;bax/bcl-2比率随浓度增加明显增高.结论 ABL-N可通过Caspase途径及bax/bcl-2蛋白途径,诱导PC3等前列腺癌细胞凋亡,抑制前列腺癌细胞增殖.
목적 탐토선복화내지(ABL)-N유도전렬선암세포조망적작용급기궤제.방법 0～40μmol/L ABL-N분별처리전렬선통세포후,이용새서람(MTF)검측대세포증장적억제작용;류식세포학、TUNEL염색등방법검측기유도조망적작용,병검측Capase활성,Western blot측정bax、bel-2수평변화.결과 ABL-N명현억제전렬선암세포PC3、LNCaP급DU145적생장,병정제량의뢰성.40 μmol/L ABL-N작용24 h후,(73.34±4.41)%적PrEC세포존활,이3충전렬선암세포분별위(11.92±2.31)%、(12.55±1.94)%、(13.28±2.26)%.막련단백/전화병정(Annexin V/PI)급TUNEL염색표명ABL-N정제량의뢰성유도PC3조망.ABL-N가격활Caspase활성,우기Caspase-3,20μmol/L ABL-N작용24 h후기활성시대조조적4.23배;bax/bcl-2비솔수농도증가명현증고.결론 ABL-N가통과Caspase도경급bax/bcl-2단백도경,유도PC3등전렬선암세포조망,억제전렬선암세포증식.
Objective To explore the ABL-N-induced apoptosis of human prostate cancer cells and the mechansim. Methods After administration of 0-40 μmol/L ABL-N for 24 h, the effects of ABL-N on the induction of apoptosis in human prostate cancer cells PC3 were measured by methyl thiazol tetrazolium ( MTT) colorimetry, Annexin V/propidium iodide staining and TUNEL staining. The levels of bax and bcl-2 were tested by Western blotting. Caspase activity was assayed. Results ABL-N treatment to PC3,LNCaP, and DU145 cells resulted in a dose-dependent inhibition of cell growth without any substantial effect on normal human prostate epithelial PrEc cells. About (73. 34 ±4. 41)% of PrEC cells were viable following a 24-h exposure to 40 μmol/L ABL-N, whereas only (11. 92 ± 2. 31) % of PC3, (12. 55 ±1. 94) % of LNcap, and (13. 28 ± 2. 26) % of DU145 cells survived under similar conditions of ABL-N treatment. ABL-N treatment resulted in a dose-dependent induction of apoptosis of PC3 cells. Furthermore,ABL-N induced the activation of Caspases, especially Caspase 3. The Caspase-3 activity of PC3 cells treated with ABL-N (20 μmol/L) (0. 95) was significantly increased by about 4. 2-fold of the untreated cells (0. 24) at 24 h. The ratio of bax/bcl-2 was also increased significantly. Conclusion ABL-N induces apoptosis though the activation of Caspase 3 and pro- and anti-apoptotic Bcl-2 family proteins in prostate cancer cells.