Ma Kaiyuan, Yuen Michael, Yuen Tina, Yuen Hywel, Peng Qiang
College of Food Science and Engineering, Northwest A&F University, Yangling, Xianyang 712100, China.
Puredia Limited, Xining 810000, China.
Antioxidants (Basel). 2024 Nov 5;13(11):1352. doi: 10.3390/antiox13111352.
Retinal pigment epithelial (RPE) is an oxidation-resistant cell. But if it is subjected to various harmful stimuli for a prolonged period, an excessive amount of oxyradical will be generated to cause retinal dysfunction. We investigated and elucidated the protective mechanism of proanthocyanidins (SBP) against oxidative damage in RPE. In this study, we established an oxidative damage model of adult retinal pigment epithelial cell line-19 (ARPE-19) using hydrogen peroxide (HO), followed by different concentrations of SBP for 24 h. The finding demonstrated that SBP effectively inhibited the generation of malondialdehyde (MDA), restored the activity of superoxide dismutase (SOD) and content of glutathione (GSH), and significantly eliminated the level of reactive oxygen species (ROS) and oxidative stress. It was revealed that 100 µg/mL of SBP was more suitable for restoring oxidative damage in ARPE-19, which enhanced cell activity and migration ability and maintained normal cell morphology. In addition, SBP increased the expression of Bcl-2, decreased the expression of Bax and caspase-3, and activated the Nrf2/HO-1 signaling pathway to protect ARPE-19 from oxidative stress. Moreover, SBP could restore the morphology and quantity of mitochondria and inhibit mitochondrial permeability and swelling. The present results provide a theoretical basis for the protective and restorative effect of SBP in retinopathy caused by oxidative stress.
视网膜色素上皮（RPE）是一种抗氧化细胞。但如果长时间受到各种有害刺激，会产生过量的氧自由基，导致视网膜功能障碍。我们研究并阐明了原花青素（SBP）对RPE氧化损伤的保护机制。在本研究中，我们用过氧化氢（HO）建立了成年视网膜色素上皮细胞系-19（ARPE-19）的氧化损伤模型，然后用不同浓度的SBP处理24小时。结果表明，SBP能有效抑制丙二醛（MDA）的生成，恢复超氧化物歧化酶（SOD）的活性和谷胱甘肽（GSH）的含量，并显著消除活性氧（ROS）水平和氧化应激。结果显示，100μg/mL的SBP更适合恢复ARPE-19中的氧化损伤，可增强细胞活性和迁移能力，并维持正常的细胞形态。此外，SBP增加了Bcl-2的表达，降低了Bax和caspase-3的表达，并激活Nrf2/HO-1信号通路以保护ARPE-19免受氧化应激。而且，SBP可恢复线粒体的形态和数量，并抑制线粒体通透性和肿胀。目前的结果为SBP在氧化应激所致视网膜病变中的保护和修复作用提供了理论依据。
