Insulin Reduces Inflammation-Related Factors Production By Suppressing Ferroptosis In Lens Epithelium Cells Under Oxidative Stress Condition
Published 2025 - 43rd Congress of the ESCRS
Reference: PO787 | Type: Free paper | DOI: 10.82333/2wbn-3j45
Authors: Pablo De Arriba Palomero* 1 , David Mingo- Botín 1 , Etxebarría Jaime 2 , Celis- Sánchez Jaime 3 , Martha Stokking 1 , Cristina García Tomás 1 , María Teresa Merino Diéz 1 , Juan Álvarez de Toledo 4 , Francisco Arnalich-Montiel 1
1Ophthalmology,Ramón y Cajal University Hospital,Madrid,Spain, 2Ophthalmology,Cruces University Hospital. ,Bilbao,Spain, 3Ophthalmology,“La Mancha-Centro” general hospital. ,Alcázar de San Juan,Spain, 4Cornea,Oftalvist,Barcelona,Spain
Purpose
Oxidative stress results in lens inflammation, thus promoting the occurrence of cataract. In recent years, the protective effect of insulin on oxidative stress and inflammation in various diseases has been gradually discovered. This study aimed to investigate the impact of insulin on oxidative stress-induced inflammation in Human Lens Epithelial Cells (HLE-B3) and elucidate the underlying mechanism through which insulin exerts its anti-inflammatory effects.
Setting
Tianjin Medical University Eye Hospital, Tianjin, China
Methods
Human anterior capsule membrane of lens including non-insulin group (I -) and insulin group(I+) were collected for Immunohistochemical staining (IHC) and immunofluorescence staining (IF) and the expression of inflammatory factors (CXCR1, CXCR2, and IL6) and ferroptosis-related protein (GPX4 and FTH1) were detected. In vitro, Western Blot, RT-qPCR, and IF were used to evaluate the effect of insulin on the expression of CXCR1, CXCR2, IL6, GPX4, and FTH1. Oil red O staining and Lipi-Green staining were utilized to measure lipid peroxide content, while FerroOrange staining was employed to determine Fe2+ content.
Results
Insulin decreased the expression of CXCR1, CXCR2, and IL-6 in HLE-B3 cells and increased the expression of GPX4 and FTH1. Additionally, insulin reduced the content of lipid peroxide and Fe2+ in HLE-B3 cells. More importantly, the reduction of ferroptosis reversed the inhibitory effect of insulin on the expression of inflammatory factors.
Conclusions
Insulin downregulates the expression of inflammatory and ferroptosis-related factors in HLE-B3 cells, potentially exerts its anti-inflammatory effect by inhibiting ferroptosis in HLE-B3 cells.