非诺贝特
氧化应激
自噬
NADPH氧化酶
糖尿病性视网膜病变
炎症
医学
糖尿病
链脲佐菌素
药理学
内分泌学
内科学
化学
细胞凋亡
生物化学
作者
Shimei Chen,Xiaoqian Wang,Dandan Sun,Shuchang Zhang,Peiyu Liu,Xun Xu,Fang Wei,Qing Liu
标识
DOI:10.1080/02713683.2025.2516802
摘要
PURPOSE: This study examines the protective effects of fenofibrate on retinal health in diabetic retinopathy, focusing on its ability to reduce inflammation, oxidative stress, and restore autophagy while preventing ferroptosis. METHODS: Using a streptozotocin (STZ)-induced diabetic rat model and cultured ARPE-19 cells under high glucose conditions, we assessed the impact of fenofibrate on oxidative stress markers, autophagy-related proteins, and tight junction integrity. Fenofibrate's role in modulating inflammation and preventing ferroptosis was also evaluated. RESULTS: Fenofibrate treatment reduced ROS production and NADPH oxidase activity, alleviating oxidative stress in retinal tissues. Additionally, fenofibrate enhanced autophagy, as indicated by increased LC3 expression, and maintained tight junction protein expression. These effects contributed to the stabilization of cellular homeostasis, potentially slowing disease progression. CONCLUSION: Fenofibrate offers significant protective effects in diabetic retinopathy by reducing inflammation and oxidative stress, promoting autophagy, and inhibiting ferroptosis, making it a promising therapeutic option for managing the disease.
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