Department of Food and Nutrition, Andong National University, Andong 36729, Republic of Korea.
Department of Food and Nutrition and Korean Institute of Nutrition, Hallym University, Chuncheon 24252, Republic of Korea.
Int J Mol Sci. 2024 Jul 17;25(14):7826. doi: 10.3390/ijms25147826.
Loss of the inner blood-retinal barrier (BRB) integrity is a main feature of ocular diseases such as diabetic macular edema. However, there is a lack of clarity on how inner BRB function is modulated within the diabetic retina. The current study examined whether eucalyptol inhibited inner BRB destruction and aberrant retinal angiogenesis in 33 mM glucose-exposed human retinal microvascular endothelial (RVE) cells and db/db mice. This study further examined the molecular mechanisms underlying endothelial dysfunction including retinal endoplasmic reticulum (ER) stress and angiopoietin (Ang)/Tie axis in conjunction with vascular endothelial growth factor (VEGF). Eucalyptol is a naturally occurring monoterpenoid and an achiral aromatic component of many plants including eucalyptus leaves. Nontoxic eucalyptol reduced the production of amyloid-β (Aβ) protein in glucose-loaded RVE cells and in diabetic mice. This natural compound blocked apoptosis of Aβ-exposed RVE cells in diabetic mouse eyes by targeting ER stress via the inhibition of PERK-eIF2α-ATF4-CHOP signaling. Eucalyptol promoted activation of the Ang-1/Tie-2 pathway and dual inhibition of Ang-2/VEGF in Aβ-exposed RVE cells and in diabetic eyes. Supply of eucalyptol reversed the induction of junction proteins in glucose/Aβ-exposed RVE cells within the retina and reduced permeability. In addition, oral administration of eucalyptol reduced vascular leaks in diabetic retinal vessels. Taken together, these findings clearly show that eucalyptol inhibits glucose-induced Aβ-mediated ER stress and manipulates Ang signaling in diabetic retinal vessels, which ultimately blocks abnormal angiogenesis and loss of inner BRB integrity. Therefore, eucalyptol provides new treatment strategies for diabetes-associated RVE defects through modulating diverse therapeutic targets including ER stress, Ang-1/Tie-2 signaling, and Ang-2/VEGF.
血视网膜内屏障 (BRB) 完整性的丧失是糖尿病性黄斑水肿等眼部疾病的主要特征。然而,对于糖尿病视网膜内 BRB 功能如何被调节,目前还缺乏清晰的认识。本研究检测了桉油精是否能抑制 33mM 葡萄糖暴露的人视网膜微血管内皮 (RVE) 细胞和 db/db 小鼠的内 BRB 破坏和异常视网膜血管生成。本研究进一步研究了内皮功能障碍的分子机制,包括视网膜内质网 (ER) 应激和血管生成素 (Ang)/Tie 轴与血管内皮生长因子 (VEGF) 结合。桉油精是一种天然存在的单萜类化合物,也是许多植物包括桉树叶的无手性芳香成分。无毒的桉油精可减少载糖的 RVE 细胞和糖尿病小鼠中淀粉样β (Aβ) 蛋白的产生。这种天然化合物通过靶向 ER 应激,通过抑制 PERK-eIF2α-ATF4-CHOP 信号通路,阻断 Aβ 暴露的 RVE 细胞在糖尿病小鼠眼中的凋亡。桉油精促进了 Ang-1/Tie-2 通路的激活,并在 Aβ 暴露的 RVE 细胞和糖尿病眼中双重抑制了 Ang-2/VEGF。桉油精的供应逆转了在葡萄糖/Aβ 暴露的 RVE 细胞中在视网膜内诱导的连接蛋白,并降低了通透性。此外,桉油精的口服给药减少了糖尿病视网膜血管中的血管渗漏。总之,这些发现清楚地表明,桉油精抑制葡萄糖诱导的 Aβ 介导的 ER 应激,并在糖尿病视网膜血管中操纵 Ang 信号,从而最终阻止异常血管生成和内 BRB 完整性的丧失。因此,桉油精通过调节包括 ER 应激、Ang-1/Tie-2 信号和 Ang-2/VEGF 在内的多种治疗靶点,为糖尿病相关的 RVE 缺陷提供了新的治疗策略。