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作 者:陈永安[1] 程蕾[2] 苗洁琼[1] 汪晨[1] 凌昌全[1]
机构地区:[1]第二军医大学附属长海医院,上海200433 [2]第二军医大学附属东方肝胆外科医院,上海200433
出 处:《福建中医药大学学报》2012年第2期22-24,共3页Journal of Fujian College of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(30901986);上海市晨光计划资助项目(10CG41)
摘 要:目的研究雷公藤甲素对人肝癌MHCC97H细胞侵袭转移的抑制作用。方法分别以50、100、200 nmol/L雷公藤甲素处理MHCC97H细胞24 h,通过细胞侵袭和迁移实验观察雷公藤甲素对MHCC97H细胞侵袭力和运动力的影响。Western-blot检测其对ERK1/2及p38信号通路活化的影响。结果侵袭实验透膜细胞数分别为(60.60±8.02)、(32.80±5.26)、(8.20±1.64),对照组为(84.40±6.88),P<0.05;迁移实验透膜细胞数分别为(172.40±14.98)、(110.20±8.26)、(24.6±3.92),对照组为(228.4±18.48),P<0.05。显示磷酸化ERK表达下调,磷酸化p38表达上调。结论雷公藤甲素具有抑制人肝癌细胞体外侵袭和转移的作用,机制可能为通过抑制ERK信号通路,活化p38信号通路。Objective To investigate the inhibitory effects of triptolide on invasion and metastasis of human liver cancer MHCC97H cells.Methods MHCC97H cells were treated with 50,100 and 200 nmol/L triptolide for 24 hours,the effects of triptolide on invasiveness and motoricity of MHCC97H cells were observed by invasion and migration assays,and its effects on the expression and activation of ERK1/2 and p38 protein were detected by Western blot.Results The number of membrane-permeating cells in observation groups was(60.60±8.02),(32.80±5.26) and(8.20±1.64) in invasion assay respectively,and in control group was(84.40±6.88)(P0.05).The number of membrane-permeating cells in observation groups was(172.40±14.98),(110.20±8.26) and(24.6±3.92) in migration assay respectively,and in control group was(228.4±18.48)(P0.05).Western blot showed that the expression of phosphorylated p38 was up-regulated and the expression of phosphorylated ERK1/2 was down-regulated.Conclusion Triptolide has inhibitory effects on invasion and metastasis of human liver cancer MHCC97H cells in vitro,and its mechanism is probably related with the effects of inhibiting ERK signal pathway and activating p38 signal pathway.
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