We evaluated whether orally administered astaxanthin (AST) protects against oxidative damage in the ocular tissues of streptozotocin (STZ)-induced diabetic rats. Fifty 6-week-old female Wistar rats were randomly assigned to receive an injection of STZ to induce diabetes (n = 40) or to remain uninduced (n = 10). The diabetic rats were randomly selected into four groups and they were separately administered normal saline, 0.6 mg/kg AST, 3 mg/kg AST, or 0.5 mg/kg lutein daily for eight weeks. Retinal functions of each group were evaluated by electroretinography. The expression of oxidative stress and inflammatory mediators in the ocular tissues was then assessed by immunohistochemistry, western blot analysis, ELISA, RT-PCR, and electrophoretic mobility shift assay (EMSA). Retinal functions were preserved by AST and lutein in different levels. Ocular tissues from AST- and lutein-treated rats had significantly reduced levels of oxidative stress mediators (8-hydroxy-2'-deoxyguanosine, nitrotyrosine, and acrolein) and inflammatory mediators (intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and fractalkine), increased levels of antioxidant enzymes (heme oxygenase-1 and peroxiredoxin), and reduced activity of the transcription factor nuclear factor-kappaB (NF-κB). The xanthophyll carotenoids AST and lutein have neuroprotective effects and reduce ocular oxidative stress, and inflammation in the STZ diabetic rat model, which may be mediated by downregulation of NF-κB activity.

Diabetic retinopathy (DR) is a common complication of diabetes that causes severe visual impairment globally. The pathogenesis of DR is related to oxidative stress and chronic inflammation. The fibroblast growth factor type 1 (FGF-1) mitogen plays crucial roles in cell function, development, and metabolism. FGF-1 is involved in blood sugar regulation and exerts beneficial antioxidative and anti-inflammatory effects on various organ systems. This study investigated the antioxidative and anti-inflammatory neuroprotective effects of FGF-1 on high-glucose-induced retinal damage. The results revealed that FGF-1 treatment significantly reversed the harmful effects of oxidative stress and inflammatory mediators in retinal tissue in a streptozotocin-induced diabetic rat model. These protective effects were also observed in the in vitro model of retinal ARPE-19 cells exposed to a high-glucose condition. We demonstrated that FGF-1 attenuated p38 mitogen-activated protein kinase and nuclear factor-κB pathway activation under the high-glucose condition. Our results indicated that FGF-1 could effectively prevent retinal injury in diabetes. The findings of this study could be used to develop novel treatments for DR that aim to reduce the cascade of oxidative stress and inflammatory signals in neuroretinal tissue.

Diabetic retinopathy (DR) severely affects vision in individuals with diabetes. High glucose (HG) induces oxidative stress in retinal cells, a key contributor to DR development. Previous studies suggest that fibroblast growth factor-1 (FGF-1) can mitigate hyperglycemia and protect tissues from HG-induced damage. However, the specific effects and mechanisms of FGF-1 on DR remain unclear. In our study, FGF-1-pretreated adult retinal pigment epithelial (ARPE)-19 cells were employed to investigate. Results indicate that FGF-1 significantly attenuated HG-induced oxidative stress, including reactive oxygen species, DNA damage, protein carbonyl content, and lipid peroxidation. FGF-1 also modulated the expression of oxidative and antioxidative enzymes. Mechanistic investigations showed that HG induced high endoplasmic reticulum (ER) stress and upregulated specific proteins associated with apoptosis. FGF-1 effectively alleviated ER stress, reduced apoptosis, and restored autophagy through the adenosine monophosphate-activated protein kinase/mammalian target of the rapamycin signaling pathway. We observed that the changes induced by HG were dose-dependently reversed by FGF-1. Higher concentrations of FGF-1 (5 and 10 ng/mL) exhibited increased effectiveness in mitigating HG-induced damage, reaching statistical significance (p < 0.05). In conclusion, our study underscores the promising potential of FGF-1 as a safeguard against DR. FGF-1 emerges as a formidable intervention, attenuating oxidative stress, ER stress, and apoptosis, while concurrently promoting autophagy. This multifaceted impact positions FGF-1 as a compelling candidate for alleviating retinal cell damage in the complex pathogenesis of DR.

To report the in vivo confocal microscopic findings of migrated melanocytes onto the central cornea in a patient with Stevens-Johnson syndrome who received ocular surface reconstruction by amniotic membrane transplantation (AMT). Single interventional case report. A 37-year-old man presented with bilateral symblepharon because of Stevens-Johnson syndrome. Release of the bilateral symblepharon with AMT on the bare sclera was performed. Three weeks after the surgery, slit-lamp biomicroscopy of the right eye revealed patchy brown pigmentation on the surface of the cornea and the amniotic membrane transplanted to the bare sclera. In vivo confocal microscopy of the affected cornea revealed abnormal basal epithelial cells with hyperreflective nuclei and loss of cellular borders. Multiple dendritiform cells, which appeared to be melanocytes, were distributed mainly on the corneal basal epithelial layer and superficial stroma. The number of the migrated melanocytes gradually decreased over 6 months of observation. Melanocytes can migrate into the central cornea after reconstruction of the ocular surface with AMT. In vivo confocal microscopy can be a useful tool to observe these changes.

PurposeTo investigate the optical coherence tomographic (OCT) patterns and long-term surgical outcomes of patients with vitreomacular traction syndrome (VMT).MethodsFrom May 2002 to April 2008, patients with OCT-confirmed VMT who underwent vitrectomy were retrospectively reviewed. Complete pre- and postoperative ophthalmic and OCT examinations were recorded. All cases were followed for at least 2 years. The OCT patterns of VMT were classified into two groups: Group 1, V-shaped macular traction (1A: without macular detachment, 1B: with macular detachment); Group 2, U-shaped macular traction (2A: without macular detachment, 2B: with macular detachment). Multiple linear regression analysis of selective factors was performed to investigate the main determinants of visual improvement.ResultsTwenty-five eyes of 25 consecutive patients were enrolled (8 in 1A, 6 in 1B, 6 in 2A, 5 in 2B). One patient in 2A progressed to 2B within 4 months. After surgery, 18 patients regained normal foveal contour accompanied by visual improvement; three patients had persistent cystoid macular edema throughout the follow-up period and a worsened visual acuity; the other four had an unchanged visual status despite improved foveal configuration. The mean ± standard deviation thickness in the central macular area was 632.0 ± 228.3 μm preoperatively and347.1 ± 126.1 μm postoperatively (p < 0.001). Multiple lineal regression analysis revealed that U-shape VMT (p = 0.005), preoperative foveal detachment (p = 0.011) and preoperative visual acuity (p = 0.035) might correlate with final vision.ConclusionOCT may detect two major configurations of VMT. Vitrectomy is an effective treatment, but U-shaped macular traction, preoperative foveal detachment and poor preoperative vision show unfavorable visual prognosis