Diabetic retinopathy (DR) is a serious neurodegenerative disease that is induced by hyperglycaemia. Oxidative stress, inflammation and endoplasmic reticulum (ER) stress are involved in the development of DR. Sulforaphane (SF) is widely found in cruciferous plants and has a protective effect against retinal neurodegeneration in diabetes, but the mechanism is unclear. In this study, we investigated the mechanism by which SF protects against photoreceptor degeneration in diabetes. In vivo, a mouse model of diabetes was established by streptozotocin (STZ) injection, and the mice were treated with/without SF. Electroretinography (ERG) and H&E staining were used to evaluate retinal function and morphology. In vitro, 661w cells were treated with AGEs with/without SF. Cell viability and apoptosis were analysed by CCK-8 assay and flow cytometry. The expression of proteins and genes was assessed by western blot and qRT-PCR. The amplitude of the a-wave was decreased and the morphology was changed in the diabetic mice, and these changes were delayed by SF treatment. The percentage of apoptotic cells was increased and the cell viability was decreased after the treatment of 661w cells with AGEs. Moreover, the expression of GRP78, Txnip and TNFα was increased, however, this increased expression was reversed by SF treatment via AMPK pathway activation. Taken together, these data show that SF can delay photoreceptor degeneration in diabetes, and the underlying mechanism is related to the inhibition of ER stress, inflammation and Txnip expression through the activation of the AMPK pathway.

中文翻译：

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萝卜硫素延​​缓糖尿病引起的视网膜感光细胞变性

糖尿病视网膜病变（DR）是一种由高血糖引起的严重的神经退行性疾病。氧化应激、炎症和内质网 (ER) 应激参与 DR 的发展。萝卜硫素（SF）广泛存在于十字花科植物中，对糖尿病视网膜神经变性具有保护作用，但机制尚不清楚。在这项研究中，我们研究了 SF 防止糖尿病光感受器变性的机制。在体内，通过链脲佐菌素（STZ）注射建立糖尿病小鼠模型，并使用/不使用SF处理小鼠。视网膜电图 (ERG) 和 H&E 染色用于评估视网膜功能和形态。在体外，661w 细胞用 AGEs 处理，有/无 SF。通过CCK-8测定和流式细胞术分析细胞活力和细胞凋亡。通过蛋白质印迹和 qRT-PCR 评估蛋白质和基因的表达。糖尿病小鼠的 a 波幅度降低，形态发生改变，SF 治疗延迟了这些变化。用AGEs处理661w细胞后，凋亡细胞百分比增加，细胞活力降低。此外，GRP78、Txnip 和 TNFα 的表达增加，然而，这种增加的表达被 SF 处理通过 AMPK 途径激活逆转。综上所述，这些数据表明SF可以延缓糖尿病光感受器变性，其潜在机制与通过激活AMPK通路抑制ER应激、炎症和Txnip表达有关。糖尿病小鼠的 a 波幅度降低，形态发生改变，SF 治疗延迟了这些变化。用AGEs处理661w细胞后，凋亡细胞百分比增加，细胞活力降低。此外，GRP78、Txnip 和 TNFα 的表达增加，然而，这种增加的表达被 SF 处理通过 AMPK 途径激活逆转。综上所述，这些数据表明SF可以延缓糖尿病光感受器变性，其潜在机制与通过激活AMPK通路抑制ER应激、炎症和Txnip表达有关。糖尿病小鼠的 a 波幅度降低，形态发生改变，SF 治疗延迟了这些变化。用AGEs处理661w细胞后，凋亡细胞百分比增加，细胞活力降低。此外，GRP78、Txnip 和 TNFα 的表达增加，然而，这种增加的表达被 SF 处理通过 AMPK 途径激活逆转。综上所述，这些数据表明SF可以延缓糖尿病光感受器变性，其潜在机制与通过激活AMPK通路抑制ER应激、炎症和Txnip表达有关。用AGEs处理661w细胞后，凋亡细胞百分比增加，细胞活力降低。此外，GRP78、Txnip 和 TNFα 的表达增加，然而，这种增加的表达被 SF 处理通过 AMPK 途径激活逆转。综上所述，这些数据表明SF可以延缓糖尿病光感受器变性，其潜在机制与通过激活AMPK通路抑制ER应激、炎症和Txnip表达有关。用AGEs处理661w细胞后，凋亡细胞百分比增加，细胞活力降低。此外，GRP78、Txnip 和 TNFα 的表达增加，然而，这种增加的表达被 SF 处理通过 AMPK 途径激活逆转。综上所述，这些数据表明SF可以延缓糖尿病光感受器变性，其潜在机制与通过激活AMPK通路抑制ER应激、炎症和Txnip表达有关。