Melissa Officinalis L. Extracts Protect Human Retinal Pigment Epithelial Cells against Oxidative Stress-Induced Apoptosis

被引:19
作者
Jeung, In Cheul [1 ,2 ]
Jee, Donghyun [3 ]
Rho, Chang-Rae [1 ,3 ]
Kang, Seungbum [1 ,3 ]
机构
[1] Catholic Univ Korea, Coll Med, Daejeon St Marys Hosp, Clin Res Inst, Daejeon 301012, South Korea
[2] Catholic Univ Korea, Dept Obstet & Gynecol, Coll Med, Seoul 137701, South Korea
[3] Catholic Univ Korea, Dept Ophthalmol & Visual Sci, Coll Med, Seoul 137701, South Korea
关键词
ALS-L1023; apoptosis; CARDIOVASCULAR-DISEASE; MACULAR DEGENERATION; HUMAN HEALTH; PATHOGENESIS; POLYPHENOLS; ACTIVATION; PREVENTION; MECHANISMS;
D O I
10.7150/ijms.13861
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: We evaluated the protective effect of ALS-L1023, an extract of Melissa officinalis L. (Labiatae; lemon balm) against oxidative stress-induced apoptosis in human retinal pigment epithelial cells (ARPE-19 cells). Methods: ARPE-19 cells were incubated with ALS-L1023 for 24 h and then treated with hydrogen peroxide (H2O2). Oxidative stress-induced apoptosis and intracellular generation of reactive oxygen species (ROS) were assessed by flow cytometry. Caspase-3/7 activation and cleaved poly ADP-ribose polymerase (PARP) were measured to investigate the protective role of ALS-L1023 against apoptosis. The protective effect of ALS-L1023 against oxidative stress through activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) was evaluated by Western blot analysis. Results: ALS-L1023 clearly reduced H2O2-induced cell apoptosis and intracellular production of ROS. H2O2-induced oxidative stress increased caspase-3/7 activity and apoptotic PARP cleavage, which were significantly inhibited by ALS-L1023. Activation of the PI3K/Akt pathway was associated with the protective effect of ALS-L1023 on ARPE-19 cells. Conclusions: ALS-L1023 protected human RPE cells against oxidative damage. This suggests that ALS-L1023 has therapeutic potential for the prevention of dry age-related macular degeneration.
引用
收藏
页码:139 / 146
页数:8
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