SERI, Switzerland Eye Research Institute, Lugano, Switzerland.
Department of Translational Research and New Technologies in Medicine and Surgery, Human Anatomy, University of Pisa, Pisa, Italy.
Curr Neuropharmacol. 2023;21(11):2227-2232. doi: 10.2174/1570159X21666230705103839.
Defective autophagy in the retinal pigment epithelium (RPE) is involved in retinal degeneration, mostly in the course of age-related macular degeneration (AMD), which is an increasingly prevalent retinal disorder, eventually leading to blindness. However, most autophagy activators own serious adverse effects when administered systemically. Curcumin is a phytochemical, which induces autophagy with a wide dose-response curve, which brings minimal side effects. Recent studies indicating defective autophagy in AMD were analyzed. Accordingly, in this perspective, we discuss and provide some evidence about the protective effects of curcumin in preventing RPE cell damage induced by the autophagy inhibitor 3-methyladenine (3-MA). Cells from human RPE were administered the autophagy inhibitor 3-MA. The cell damage induced by 3-MA was assessed at light microscopy by hematoxylin & eosin, Fluoro Jade-B, and ZO1 immunohistochemistry along with electron microscopy. The autophagy inhibitor 3-MA produces cell loss and cell degeneration of RPE cells. These effects are counteracted dose-dependently by curcumin. In line with the hypothesis that the autophagy machinery is key in sustaining the integrity of the RPE, here we provide evidence that the powerful autophagy inhibitor 3-MA produces dose-dependently cell loss and cell degeneration in cultured RPE cells, while inhibiting autophagy as shown by LC3-II/LC3-I ratio and gold-standard assessment of autophagy through LC3-positive autophagy vacuoles. These effects are prevented dose-dependently by curcumin, which activates autophagy. These data shed the perspective of validating the role of phytochemicals as safe autophagy activators to treat AMD.
视网膜色素上皮 (RPE) 中的自噬缺陷与视网膜变性有关,主要发生在年龄相关性黄斑变性 (AMD) 过程中,AMD 是一种日益流行的视网膜疾病,最终导致失明。然而,大多数自噬激活剂在全身给药时都有严重的不良反应。姜黄素是一种植物化学物质,它可以诱导自噬,具有较宽的剂量反应曲线,副作用极小。最近的研究表明 AMD 中存在自噬缺陷。因此,在这方面,我们讨论并提供了一些关于姜黄素在预防自噬抑制剂 3-甲基腺嘌呤 (3-MA) 诱导的 RPE 细胞损伤中的保护作用的证据。用人 RPE 细胞给予自噬抑制剂 3-MA。通过苏木精和伊红、荧光 Jade-B 和 ZO1 免疫组织化学以及电子显微镜评估 3-MA 诱导的细胞损伤。自噬抑制剂 3-MA 导致 RPE 细胞的细胞丢失和细胞变性。姜黄素可以剂量依赖性地拮抗这些作用。与自噬机制对于维持 RPE 完整性至关重要的假设一致,我们在这里提供证据表明,强大的自噬抑制剂 3-MA 以剂量依赖性方式导致培养的 RPE 细胞丢失和细胞变性,同时通过 LC3-II/LC3-I 比值和通过 LC3 阳性自噬空泡进行自噬的金标准评估来抑制自噬。姜黄素可以剂量依赖性地预防这些作用,姜黄素可以激活自噬。这些数据为验证植物化学物质作为安全自噬激活剂治疗 AMD 的作用提供了新的视角。