摘要
目的:探讨线粒体膜电位(△ψm)、Caspase 3在As2O3诱导ACC-2细胞凋亡中的作用。方法:进行ACC-2细胞培养,将As2O3建立不同药物浓度梯度(0,1.0,2.0,4.0,8.0μmol/L)分别作用于ACC-2细胞,用Rh123染色,流式细胞仪检测8.0μmol/L As2O3作用前、后(24h),ACC-2细胞的线粒体膜电位(△ψm)变化;用多功能酶标仪进行Caspase 3活性检测。结果:空白对照组ACC-2细胞内Rh123荧光强度最强,8.0μmol/L As2O3处理组ACC-2细胞内Rh123荧光强度减弱,其差异有显著性(P<0.05);随着As2O3药物浓度的增高(0,1,2,4,8μmol/L),ACC-2细胞的Caspase 3酶活力单位逐渐增加。结论:As2O3作用于ACC-2细胞,可通过降低线粒体膜电位从而引起细胞凋亡。随着As2O3药物浓度的增高,ACC-2细胞的Caspase 3酶活力单位逐渐增加,Caspase 3被激活,细胞可发生不可逆转的凋亡过程。
AIM： To investigate the membrane potential （△ψm） and cell apoptosis induced by As203. role of mitochondrial Caspase 3 in the ACC-2 METHODS： ACC-2 cells were cultured. The As2 03 of different drug concentration gradients （0, 1.0, 2.0, 4.0, 8.0wmol/L） were applied to ACC-2 cells respectively. The changes in △ψm of ACC-2 cells before and after As2 O3＇s inducing （8.0w mol/L for 24h） were detected by flow cytometry with Rh123 staining. Caspase 3 activity was detected by the multifunctional microplate reader. RESULTS： Rh123 fluorescence intensity in ACC-2 cells was strongest in the control group, while it weakened in ACC-2 cells in 8.0wmol/L As203 treatment group. The difference between two groups was significant （P〈0.05）. With the increase of As2 03 concentration （0, 1. 0, 2.0, 4. 0, 8.0p mol/L）, Caspase 3 enzyme activity unit in ACC-2 cells gradually increased. CONCLUSION ： As2 03 can induce apoptosis of ACC- 2 cells by reducing △ψm. Caspase 3 enzyme activity unit of ACC-2 cells gradually increases with As2 03 concentration increases, which results in activation of the expression of Caspase 3, and the cells＇ irreversible apoptosis process coming immediately.
出处
《国际眼科杂志》
CAS
2014年第2期232-235,共4页
International Eye Science
基金
山东省自然科学基金资助项目(No.ZR2012HM062)~~
作者简介
欧阳艳艳，在读硕士研究生，研究方向：眼外伤、眼底病、眼眶病。通讯作者：姜涛，博士，副教授，硕士研究生导师，副主任医师，副主任，研究方向：眼外伤、眼底病、角膜病、白内障、眼眶病．1anlandetian20000@163．com
