Hyperglycemia elicits tight junction disruption and blood-retinal barrier breakdown, resulting in diabetes-associated vison loss. Eucalyptol is a natural compound found in eucalyptus oil with diverse bioactivities. This study evaluated that eucalyptol ameliorated tight junctions and retinal barrier function in glucose/amyloid-β (Aβ)-exposed human retinal pigment epithelial (RPE) cells and in db/db mouse eyes. RPE cells were cultured in media containing 33 mM glucose or 5 μM Aβ for 4 days in the presence of 1–20 μM eucalyptol. The in vivo animal study employed db/db mice orally administrated with 10 mg/kg eucalyptol. Nontoxic eucalyptol inhibited the Aβ induction in glucose-loaded RPE cells and diabetic mouse eyes. Eucalyptol reversed the induction of tight junction-associated proteins of ZO-1, occludin-1 and matrix metalloproteinases in glucose- or Aβ-exposed RPE cells and in diabetic eyes, accompanying inhibition of RPE detachment from Bruch’s membrane. Adding eucalyptol to glucose- or Aβ-loaded RPE cells, and diabetic mouse eyes reciprocally reversed induction/activation of apoptosis-related bcl-2, bax, cytochrome C/Apaf-1 and caspases. Eucalyptol attenuated the generation of reactive oxygen species and the induction of receptor for advanced glycation end products in Aβ-exposed RPE cells and diabetic eyes. Eucalyptol may ameliorate RPE barrier dysfunction in diabetic eyes through counteracting Aβ-mediated oxidative stress-induced RPE cell apoptosis.

中文翻译：

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桉树油抑制葡萄糖暴露的视网膜色素上皮细胞和糖尿病眼中淀粉样β诱导的屏障功能障碍。

高血糖症会引起紧密的连接破坏和血视网膜屏障破坏，从而导致糖尿病相关的vison丢失。桉树油是在桉树油中发现的具有多种生物活性的天然化合物。这项研究评估了桉树油改善了暴露于葡萄糖/淀粉样β（Aβ）的人视网膜色素上皮（RPE）细胞和db / db小鼠眼中的紧密连接和视网膜屏障功能。RPE细胞在含有1-20μM桉树精的情况下，在含有33 mM葡萄糖或5μMAβ的培养基中培养4天。体内动物研究使用了口服10 mg / kg桉树素的db / db小鼠。无毒桉树油抑制葡萄糖加载的RPE细胞和糖尿病小鼠眼睛中的Aβ诱导。桉树脑逆转了ZO-1紧密连接相关蛋白的诱导，暴露于葡萄糖或Aβ的RPE细胞和糖尿病眼中的occludin-1和基质金属蛋白酶，同时抑制了RPE从Bruch膜上脱离。向负载葡萄糖或Aβ的RPE细胞中添加桉树油和糖尿病小鼠眼，可逆转与凋亡相关的bcl-2，bax，细胞色素C / Apaf-1和胱天蛋白酶的诱导/激活。桉树油减弱了暴露于Aβ的RPE细胞和糖尿病眼中活性氧的产生以及晚期糖基化终产物受体的诱导。桉树油可以通过抵抗Aβ介导的氧化应激诱导的RPE细胞凋亡来改善糖尿病眼中的RPE屏障功能障碍。糖尿病小鼠的眼睛则逆转了与凋亡相关的bcl-2，bax，细胞色素C / Apaf-1和胱天蛋白酶的诱导/激活。桉树油减弱了暴露于Aβ的RPE细胞和糖尿病眼中活性氧的产生以及晚期糖基化终产物受体的诱导。桉树油可以通过抵抗Aβ介导的氧化应激诱导的RPE细胞凋亡来改善糖尿病眼中的RPE屏障功能障碍。糖尿病小鼠的眼睛则逆转了与凋亡相关的bcl-2，bax，细胞色素C / Apaf-1和胱天蛋白酶的诱导/激活。桉树油减弱了暴露于Aβ的RPE细胞和糖尿病眼中活性氧的产生以及晚期糖基化终产物受体的诱导。桉树油可以通过抵抗Aβ介导的氧化应激诱导的RPE细胞凋亡来改善糖尿病眼中的RPE屏障功能障碍。