Aims

The objectives of this study were to explore physiological and pathological changes in the corneas of diabetic rats by intervening in the expression of silent information regulator 1 (Sirt1) and to investigate whether Sirt1 can regulate the activation of endoplasmic reticulum stress (ERS) while influencing corneal epithelial cell apoptosis under high glucose conditions.

Materials and methods

Using 8-week old Sprague-Dawley rats, we established a model of type 1 diabetes, with or without Sirt1 intervention. Clinical evaluation was performed once per week. Primary rat corneal epithelial cells (RCECs) were cultured by combining Sirt1 intervention under high glucose conditions. Generation of reactive oxygen species (ROS), apoptosis, and the expression of Sirt1 and ERS-related proteins were evaluated in rat corneal tissues and RCECs.

Key findings

During the intervention, clinical evaluation of the ocular surface, ROS generation, apoptosis, and protein expression of ERS-related proteins in corneal tissue and cultured RCECs were altered with Sirt1expression levels.

Significance

Sirt1 expression influences the pathological progression of diabetic keratopathy, plays an important role in regulating the ERS pathway, and decreases corneal epithelial cell apoptosis.

中文翻译：

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Sirt1通过调节内质网应激途径减轻糖尿病性角膜病变

目的

这项研究的目的是通过干预沉默信息调节因子1（Sirt1）的表达来探索糖尿病大鼠角膜的生理和病理变化，并研究Sirt1是否可以在影响角膜的同时调节内质网应激（ERS）的激活。高糖条件下上皮细胞凋亡

材料和方法

使用8周大的Sprague-Dawley大鼠，我们建立了有或没有Sirt1干预的1型糖尿病模型。每周进行一次临床评估。通过在高葡萄糖条件下结合Sirt1干预培养原代大鼠角膜上皮细胞（RCEC）。在大鼠角膜组织和RCEC中评估了活性氧（ROS）的生成，细胞凋亡以及Sirt1和ERS相关蛋白的表达。

主要发现

在干预过程中，随着Sirt1表达水平的改变，眼表，ROS生成，细胞凋亡以及ERS相关蛋白在角膜组织和培养的RCEC中的蛋白表达的临床评估会发生变化。

意义

Sirt1表达影响糖尿病性角膜病变的病理进展，在调节ERS通路中起重要作用，并减少角膜上皮细胞凋亡。