首页> 外文期刊>International Journal of Medical Sciences >Melissa Officinalis L. Extracts Protect Human Retinal Pigment Epithelial Cells against Oxidative Stress-Induced Apoptosis
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Melissa Officinalis L. Extracts Protect Human Retinal Pigment Epithelial Cells against Oxidative Stress-Induced Apoptosis

机译:蜜蜂花提取物保护人类视网膜色素上皮细胞免受氧化应激诱导的细胞凋亡。

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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.
机译:背景:我们评估了蜜蜂花提取物ALS-L1023(唇形科;柠檬香脂)的提取物对氧化应激诱导的人视网膜色素上皮细胞(ARPE-19细胞)凋亡的保护作用。方法:将ARPE-19细胞与ALS-L1023一起培养24 h,然后用过氧化氢(H 2 O 2 )处理。通过流式细胞仪评估氧化应激诱导的细胞凋亡和细胞内生成的活性氧(ROS)。测量Caspase-3 / 7激活和裂解的聚ADP-核糖聚合酶(PARP),以研究ALS-L1023对细胞凋亡的保护作用。通过蛋白质印迹分析评估了ALS-L1023通过激活磷脂酰肌醇3-激酶/蛋白激酶B(PI3K / Akt)对氧化应激的保护作用。结果:ALS-L1023明显减少了H 2 O 2 诱导的细胞凋亡和细胞内ROS的产生。 H 2 O 2 诱导的氧化应激增加了caspase-3 / 7活性和凋亡PARP裂解,这被ALS-L1023明显抑制。 PI3K / Akt途径的激活与ALS-L1023对ARPE-19细胞的保护作用有关。结论:ALS-L1023保护人RPE细胞免受氧化损伤。这表明ALS-L1023具有预防与干龄相关的黄斑变性的治疗潜力。

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