Department of Ophthalmology, St. Marianna University School of Medicine, Kawasaki, Kanagawa 216‑8511, Japan.
Mol Med Rep. 2018 Dec;18(6):5455-5460. doi: 10.3892/mmr.2018.9568. Epub 2018 Oct 22.
Beclin‑1 serves a pivotal role in autophagosome formation. A previous study demonstrated that streptozotocin‑induced hyperglycemia (HG) ameliorates axonal loss induced by tumor necrosis factor (TNF) with upregulation of autophagy in rats. The aim of present study was to examine whether Beclin‑1 is involved in this autophagy machinery. Immunoblot analysis of optic nerves demonstrated that HG upregulated Beclin‑1 protein expression when compared with normoglycemia (NG). Intravitreal administration of TNF did not alter the optic nerve Beclin‑1 expression in NG nor in HG. Beclin‑1 immunoreactivity was revealed to be mainly in astrocytes in optic nerves; however, it was also observed in the neurofilaments of the HG group. Morphometric analysis revealed that HG appeared to have substantial ameliorative effects on axon loss and this ameliorative effect was partially prevented by Beclin‑1 small interfering RNA. These results indicated that Beclin‑1 may exist in neurons and glia in optic nerves and increased Beclin‑1 expression may be at least partially associated with axonal protection by HG.
Beclin-1 在自噬体形成中起关键作用。先前的一项研究表明，链脲佐菌素诱导的高血糖症 (HG) 通过上调大鼠中的自噬来减轻肿瘤坏死因子 (TNF) 诱导的轴突丢失。本研究旨在研究 Beclin-1 是否参与这种自噬机制。视神经的免疫印迹分析表明，与正常血糖 (NG) 相比，HG 上调了 Beclin-1 蛋白表达。在 NG 和 HG 中，眼内注射 TNF 并未改变视神经 Beclin-1 的表达。Beclin-1 免疫反应性主要在视神经中的星形胶质细胞中显现；然而，在 HG 组中也观察到了神经丝。形态计量学分析表明，HG 似乎对轴突丢失有实质性的改善作用，而 Beclin-1 小干扰 RNA 部分阻止了这种改善作用。这些结果表明，Beclin-1 可能存在于视神经中的神经元和神经胶质细胞中，并且 Beclin-1 表达的增加至少部分与 HG 诱导的轴突保护有关。
