Effects of UVB-induced damage on corneal tissues in surgical menopause female rats by bilaterally ovariectomy

Background aims: Menopause is associated with increased production of inflammatory cytokines, such as TNF-α and TGF-β. The elevated cytokine levels likely contribute to the increased incidence of inflammatory diseases after menopause, such as osteoporosis, and neurodegenerative cardiovascular diseases and visual disease. To determine the role of 17β-estradiol and involvement of its receptors in the prevention of light-induced corneal disorders, we performed oxidative UVB-induced corneal injury model following surgically ovariectomized (OVX) female rats. Effects of UVB-induced damage on corneal tissues in OVX were compared to that in no OVX female animals. Methods: Fifteen female Sprague-Dawley rats were randomly divided into three groups. Corneal oxidative injury was induced by exposure to UVB irradiation at 560 μW/cm² for five days, followed surgical menopause induced by bilaterally OVX. The experimental animals without surgically OVX were used as surgical treatment controls and animals without UVB irradiation as blank controls. Leukocyte accumulation and central corneal epithelial thickness after injury were examined by histopathology analysis, respectively. Results: UVB irradiation caused substantial damage to the corneas, including thinning of corneal epithelial layer, induction of neovasculazation. After surgical menopause by bilaterally ovariectomy, corneal disorders were significantly enhanced compared with UVB and blank control groups. Studies showed that increased central corneal epithelial disorders and corneal neovasculazation after ovariectomy in vivo in terms of change in corneal epithelial thickness and vessel length (P