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Resolvin D1 reduces mitochondrial damage to photoreceptors of primary retinal cells exposed to high glucose

机译:Resolvin D1减少线粒体损伤基本视网膜光感受器细胞暴露高葡萄糖

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No study has investigated the interaction of Resolvin Dl (RvD1) with mitochondrial damage of retinal cells caused by diabetes. This study aims to investigate the effects of RvD1 (50 nM) on morphological and biochemical indicators of mitochondrial damage in primary retinal cells exposed to 30 mM D-glucose high glucose (HG). HG-cells exhibited photoreceptor damage characterized by short and small mitochondria with prevalent mitochondrial disruption, fragmentation, and aggregation. The cells had low mitochondrial transporters TIMM44 and TOMM40, Connexin 43, NAD/NADH ratio, and ATP levels, whereas increased cytosolic cytochrome c. Moreover, they expressed high cytosolic metalloproteinase matrix metallopeptidase 9 (MMP-9) and MMP-2 activity. HG-cells treated with RvD1 (50 nM) showed reduced reactive oxygen species levels, improved mitochondrial morphology and function, promoted mitochondrial DNA repair by OGG1, and reduced cell apoptosis and metalloproteinase activity. Therefore, RvD1 induces protection from high glucose-load to the retinal cell and promotes their survival by decreasing cytosolic MMP and mitochondrial damage.
机译:没有研究调查之间的相互作用Resolvin Dl (RvD1)与线粒体损伤糖尿病引起的视网膜细胞。调查的影响RvD1(50海里)形态学和生化指标线粒体损伤的视网膜细胞接触到30毫米葡萄糖高葡萄糖(HG)。HG-cells展出光感受器损伤特点是短而小的线粒体与普遍的线粒体中断,分裂和聚合。线粒体的转运蛋白TIMM44 TOMM40,联接蛋白43、NAD / NADH比率和ATP的水平,而增加胞质细胞色素c。此外,他们表达了胞质高基质金属蛋白酶metallopeptidase 9(MMP-9)和MMP-2活动。RvD1 (50 nM)显示减少活性氧物种水平,改善线粒体形态和功能,促进了线粒体DNA修复OGG1,减少细胞凋亡金属蛋白酶活性。从高糖负荷诱发保护视网膜细胞,促进他们的生存减少胞质MMP和线粒体损害。

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