Protective Effects of Verapamil against H2O2-Induced Apoptosis in Human Lens Epithelial Cells.
10.4062/biomolther.2014.033
- Author:
Zhuo WANG
1
;
Dan WANG
;
Yan LI
;
Xiuli ZHANG
Author Information
1. School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, Shandong, 264003, P.R.China. zhangxiuli2008@163.com
- Publication Type:Original Article
- Keywords:
Apoptosis;
Caspase-3;
Human lens epithelial cell;
Verapamil
- MeSH:
Angina Pectoris;
Apoptosis*;
Atrial Fibrillation;
Bisbenzimidazole;
Caspase 3;
Cell Culture Techniques;
Cell Death;
Epithelial Cells*;
Flow Cytometry;
Glutathione;
Humans;
Hypertension;
Immunohistochemistry;
Optic Disk;
Oxidative Stress;
RNA, Messenger;
Verapamil*
- From:Biomolecules & Therapeutics
2014;22(6):553-557
- CountryRepublic of Korea
- Language:English
-
Abstract:
Verapamil is used in the treatment of hypertension, angina pectoris, and atrial fibrillation. Recently, several studies have demonstrated that verapamil increased the optic nerve head blood flow and improved the retrobulbar circulation. All these show that verapamil is potentially useful for ophthalmic treatment. Thus, the aim of this study is to investigate whether verapamil could protect human lens epithelial cell (HLEC) from oxidative stress induced by H2O2 and the cellular mechanism underlying this protective function. The viability of HLEC was determined by the MTT assay and apoptotic cell death was analyzed by Hoechst 33258 staining. Moreover, Caspase-3 expression was detected by immunocytochemistry and flow cytometry analysis. We also detected Caspase-3 mRNA expression by reverse-transcription-polymerase chain reaction and the GSH content in cell culture. The results showed that oxidative stress produced significant cell apoptotic death and it was reduced by previous treatment with the verapamil. Verapamil was effective in reducing HLEC death mainly through reducing the expression level of apoptosis-related proteins, caspase-3, and increasing glutathione content. Therefore, it was suggested that verapamil was effective in reducing HLEC apoptosis induced by H2O2.
