Improved effect of a mitochondria-targeted antioxidant on hydrogen peroxide-induced oxidative stress in human retinal pigment epithelium cells.

Improved effect of a mitochondria-targeted antioxidant on hydrogen peroxide-induced oxidative stress in human retinal pigment epithelium cells.
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DOI:
10.1186/s40360-020-00471-w
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发表时间:
2021-01-20
影响因子:
2.9
通讯作者:
Kim DY
Kim DY
中科院分区:
医学4区
文献类型:
--
作者:
Kim MH;Kim DH;Yang SG;Kim DY

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视网膜色素上皮(RPE)细胞的氧化损伤有助于年龄相关性黄斑变性的发展,这是老年人视力丧失的主要原因之一。在本研究中,我们评估了三苯基磷(TPP)-烟酸对过氧化氢(H2 O2)诱导的RPE细胞氧化应激的保护作用。在H2 O2处理或用TPP-Niacin预处理的情况下,测定视网膜ARPE-19细胞的细胞活力、乳酸脱氢酶释放、活性氧(ROS)产生和线粒体功能。采用实时荧光定量聚合酶链反应(RT-qPCR)检测线粒体相关基因和转录因子的表达水平。TPP烟酸显着提高细胞活力,减少ROS的产生,并增加过氧化氢处理的ARPE-19细胞中的抗氧化酶。由H2 O2诱导的氧化应激引起的线粒体功能障碍也被TPP-烟酸处理显著减少,沿着线粒体膜电位(MMP)降低和线粒体相关基因上调。此外,TPP-Niacin还能显著增强转录因子PGC-1α和NRF 2以及抗氧化相关基因HO-1和NQO-1的表达。我们验证了TPP-烟酸对H2 O2诱导的RPE细胞氧化应激的保护作用。据信,TPP-烟酸通过上调RPE细胞中的抗氧化剂相关基因(如PGC-1α、NRF 2、HO-1和NQO-1)来防止线粒体功能障碍。在线版本包含补充材料,可通过10.1186/s40360-020-00471-w获得。
Oxidative damage to retinal pigment epithelial (RPE) cells contributes to the development of age-related macular degeneration, which is among the leading causes of visual loss in elderly people. In the present study, we evaluated the protective role of triphenylphosphonium (TPP)-Niacin against hydrogen peroxide (H2O2)-induced oxidative stress in RPE cells. The cellular viability, lactate dehydrogenase release, reactive oxygen species (ROS) generation, and mitochondrial function of retinal ARPE-19 cells were determined under treatment with H2O2 or pre-treatment with TPP-Niacin. The expression level of mitochondrial related genes and some transcription factors were assessed using real-time polymerase chain reaction (RT-qPCR). TPP-Niacin significantly improved cell viability, reduced ROS generation, and increased the antioxidant enzymes in H2O2-treated ARPE-19 cells. Mitochondrial dysfunction from the H2O2-induced oxidative stress was also considerably diminished by TPP-Niacin treatment, along with reduction of the mitochondrial membrane potential (MMP) and upregulation of the mitochondrial-associated gene. In addition, TPP-Niacin markedly enhanced the expression of transcription factors (PGC-1α and NRF2) and antioxidant-associated genes (especially HO-1 and NQO-1). We verified the protective effect of TPP-Niacin against H2O2-induced oxidative stress in RPE cells. TPP-Niacin is believed to protect against mitochondrial dysfunction by upregulating antioxidant-related genes, such as PGC-1α, NRF2, HO-1, and NQO-1, in RPE cells. The online version contains supplementary material available at 10.1186/s40360-020-00471-w.
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