Sirt1 attenuates diabetic keratopathy by regulating the endoplasmic reticulum stress pathway

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.