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Updated: May 12, 2026

An Epithelial Abrasion Model for Studying Corneal Wound Healing
Published on: December 29, 2021
17β-Estradiol accelerates corneal epithelial repair associated with anti-inflammatory and pro-regenerative molecular
G Usta Sofu1, U Karaca2, Y Erzurumlu3
1Department of Ophthalmology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
Background:
This study aimed to investigate the effects of topical 17β-estradiol (E2) administration on the rate of corneal epithelial wound healing and the modulation of key inflammatory (IL-1β, TNF-α) and regenerative (VEGF, E-cadherin, and KGF) markers in a rat model of corneal abrasion (ABR).
Materials And Methods:
Thirty-two male Wistar Albino rats were divided into four groups (n = 8 eyes/group): Control, ABR, ABR+E2, and E2. A central 5-mm corneal epithelial abrasion was performed in the ABR and ABR+E2 groups. Topical E2 was administered five times daily to the ABR+E2 and E2 groups. Clinical healing was assessed 24 h post-injury. At 72 h, the expression of IL-1β, TNF-α, and VEGF was evaluated via immunohistochemistry, while E-cadherin and KGF mRNA levels were analyzed using RT-qPCR.
Results:
Topical E2 treatment significantly reduced the corneal epithelial defect from 4.2 ± 0.3 mm² in the ABR group to 2.8 ± 0.4 mm² in the ABR+E2 group (p < 0.01) within 24 h. At 72 h, histopathological analysis showed a reduction in tissue damage scores from a median of 7.0 (IQR: 2.0) in the ABR group to 4.0 (IQR: 2.5) in the ABR+E2 group, though this reduction did not reach statistical significance (p > 0.05). In contrast, E2 administration significantly reduced IL-1β (Median: 1.0, p < 0.01) and TNF-α (Median: 2.0, p < 0.05) expression compared to the ABR group. Furthermore, E2 treatment significantly increased VEGF levels (Median: 2.0, p < 0.05) compared to the ABR group (Median: 1.0). RT-qPCR results demonstrated that the ABR+E2 group had significantly higher E-cadherin (p = 0.002) and KGF (p = 0.015) mRNA levels compared to the ABR group. Comparative analysis showed that E-cadherin expression in the ABR+E2 group was statistically comparable to the E2 group (p = 0.742), and KGF expression was statistically indistinguishable from the Control group (p = 0.138).
Conclusions:
Topical E2 facilitates rapid corneal repair by modulating IL-1β and TNF-α mediated inflammation and restoring the expression of key regenerative markers, including E-cadherin, KGF, and VEGF, to physiological levels. These findings suggest that E2 is a potent anti-inflammatory and pro-regenerative therapeutic candidate for the clinical management of acute corneal injuries.

