内质网应激机制在虾青素作用下的CBRH-7919细胞中的调控  

Regulation of endoplasmic reticulum stress in CBRH-7919 cell under astaxanthin

作　　者：宋晓冬[1] 刘文波[1] 张瑾锦[1] 王秀文[1] 王斌[1] 

机构地区：[1]滨州医学院实验中心,烟台市264003

出　　处：《滨州医学院学报》2009年第6期401-404,共4页Journal of Binzhou Medical University

基　　金：山东省软科学研究计划项目(2008RK185);滨州医学院大学生活动创新基金(BY2007DKCX10)

摘　　要：目的通过检测虾青素(Astaxanthin)对大鼠肝癌CBRH-7919细胞内质网应激机制的影响,从海洋活性成分中筛选抗肝癌的药物。方法CBRH-7919细胞分为空白对照组、70μmol/ml虾青素作用12 h组、24 h组,光镜下观察细胞形态变化,透射电子显微镜下观察细胞内质网变化,倒置荧光显微镜下观测Fura-2 AM标记的Ca2+荧光强度变化,流式细胞仪检测RH-123标记的线粒体跨膜电位变化。结果虾青素作用后,细胞变形、贴壁松弛,内质网脱颗粒,线粒体膜、核膜等膜结构破碎,Ca2+浓度升高,线粒体跨膜电位降低。结论虾青素能够抑制CBRH-7919细胞的生长,这可能是由于虾青素引起细胞内质网应激机制,长期过强的应激启动了细胞死亡通路,导致了细胞死亡。Objective To probe into the effect of astaxanthin on endoplasmic reticulum stress in CBRH-7919 cell for selective antitumour activity in hepatocellular carcinoma.Methods The cells were divided into 3 groups as following：control group,test group with 70μmol/ml astaxanthin for 12 hours and 24 hours.Observed the cell morphological with light microscope.Revealed the cell endoplasmic reticulum under transmission electron microscope.Detected the fluorescence intensity of Ca2＋ in the cell marked by Fura-2 AM with the inverted fluorescence microscope.Measured the mitochondrial transmembrane potential marked RH-123 with flow cytometry.Results Under the astaxanthin,cells were out of shape,relaxation adherent and degranulation of endoplasmic reticulum.The membrane structure such as nuclear envelope,mitochondrial membrane broken or loose.Calcium concentration was increased,but mitochondrial transmembrane potential was reduced.Conclusion Astaxanthin could inhibit rat hepatoma cells.The mechanism was possibly related to endoplasmic reticulum stress which induced cell death.

关 键 词：虾青素 内质网 CA2+ 线粒体跨膜电位 

分 类 号：R979.1[医药卫生—药品]