Deppe Leonie, Mueller-Buehl Ana M, Tsai Teresa, Erb Carl, Dick H Burkhard, Joachim Stephanie C
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
Private Institute for Applied Ophthalmology, Eye Clinic at Wittenbergplatz, 10787 Berlin, Germany.
J Pers Med. 2024 Apr 22;14(4):437. doi: 10.3390/jpm14040437.
Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (HO) in a porcine organ culture model. Retinal explants were cultivated for eight days, and HO (500 µM, 3 h) induced the oxidative damage. CoQ10 therapy was applied (700 µM, 48 h). Retinal ganglion cells (RGCs) and microglia were examined immunohistologically in all groups (control, HO, HO + CoQ10). Cellular, oxidative, and inflammatory genes were quantified via RT-qPCR. Strong RGC loss was observed with HO ( ≤ 0.001). CoQ10 elicited RGC protection compared to the damaged group at a histological ( ≤ 0.001) and mRNA level. We detected more microglia cells with HO, but CoQ10 reduced this effect ( = 0.004). Cellular protection genes () against oxidative stress were stimulated by CoQ10 ( ≤ 0.001). Furthermore, mitochondrial oxidative stress () increased through HO ( = 0.038), and CoQ10 reduced it to control level. Our novel results indicate neuroprotection via CoQ10 in porcine retina organ cultures. In particular, CoQ10 appears to protect RGCs by potentially inhibiting apoptosis-related pathways, activating intracellular protection and reducing mitochondrial stress.
氧化应激在包括青光眼在内的神经退行性疾病中起重要作用。因此，我们分析了同样可在市场上买到的抗氧化剂辅酶Q10（CoQ10）是否能在猪器官培养模型中预防过氧化氢（HO）诱导的视网膜变性。视网膜外植体培养8天，HO（500µM，3小时）诱导氧化损伤。应用CoQ10治疗（700µM，48小时）。对所有组（对照组、HO组、HO + CoQ10组）的视网膜神经节细胞（RGCs）和小胶质细胞进行免疫组织学检查。通过RT-qPCR对细胞、氧化和炎症基因进行定量分析。HO组观察到明显的RGC损失（≤0.001）。与受损组相比，CoQ10在组织学（≤0.001）和mRNA水平上对RGCs具有保护作用。我们检测到HO组的小胶质细胞更多，但CoQ10减轻了这种效应（=0.004）。CoQ10刺激了对抗氧化应激的细胞保护基因（≤0.001）。此外，HO导致线粒体氧化应激增加（=0.038），而CoQ10将其降低至对照水平。我们的新结果表明CoQ在猪视网膜器官培养中具有神经保护作用。特别是，CoQ10似乎通过潜在地抑制凋亡相关途径、激活细胞内保护和减轻线粒体应激来保护RGCs。
