辛伐他汀对结肠癌细胞HCT116凋亡的诱导作用及其机制  

Apoptosis-inducing effect and the mechanism of Simvastatin on colon cancer cell line HCT116

作　　者：陈勇[1] 朱洁[1] 张斌[1] 王英英 鲁兰[1] 唐春艳[1] CHEN Yong;ZHU Jie;ZHANG Bin;WANG Yingying;LU Lan;TANG Chunyan(Antibiotics Research and Re-evaluation Key Laboratory of Sichuan Province,Sichuan Industrial Institute of Antibiotics,School of Pharmacy,Chengdu University,Chengdu,Sichuan,610106 P.R.China)

机构地区：[1]成都大学药学院四川抗菌素工业研究所抗生素研究与再评价四川省重点实验室,四川成都610106

出　　处：《华西药学杂志》2022年第1期29-31,共3页West China Journal of Pharmaceutical Sciences

基　　金：国家自然科学基金资助项目(批准号:81803812)。

摘　　要：目的观察辛伐他汀对结肠癌细胞HCT116凋亡的诱导作用,初探其可能机制。方法采用MTT法测定辛伐他汀对小鼠结肠癌细胞株HCT116生长的抑制作用;用Western blot法测定辛伐他汀对细胞凋亡相关蛋白PARP、cleaved-PARP和KLF2、KLF4以及细胞增殖相关蛋白P21、P-P53表达的影响情况。结果辛伐他汀对小鼠结肠癌细胞HCT116的生长具明显抑制作用;凋亡标志蛋白cleaved-PARP的水平明显上升;阻断AMPK信号途径可明显抑制辛伐他汀对cleaved-PARP蛋白的诱导作用。结论辛伐他汀具有明显的抗肿瘤作用,可能与AMPK信号途径有关。OBJECTIVE To investigate apoptosis-inducing effect and mechanism of Simvastatin(Sim)on colon cancer cell line HCT116.METHODS MTT assay was used to determine the inhibitory effect of Sim on the growth of mouse colon cancer cell line HCT116;Western blot was used to detect the effects of Sim on the expression of proteins including apoptosis-related protein such as PARP and cleaved-PARP,KLF2 and KLF4,proliferation-related p21 and phosphorylated p53.RESULTS Sim significantly inhibited the growth of HCT116 cells and increased the level of cleaved-PARP in HCT116 cells.Blocking AMPK signaling pathway could significantly inhibit the induction of cleaved-PARP protein by Sim.CONCLUSION Sim exerts a significant antitumor effect,may be related to AMPK signaling pathway.

关 键 词：辛伐他汀 结肠癌细胞 cleaved-PARP蛋白 AMPK信号途径 细胞凋亡 抗肿瘤作用 HCT116 肿瘤代谢 

分 类 号：R96[医药卫生—药理学]