Indian Journal of Ophthalmology最新文献

Purpose: Age-related cataract (ARC) is one of the leading causes of blindness and visual impairment globally. The aim of this study was to explore the role of Notch 3 in ARC as well as the mechanisms underlying Notch 3 in ARC.

Methods: An in vitro model was established to mimick the microenvironment of ARC, the lens epithelial cell line (LEC) B3 were treated with hydrogen peroxide (H2O2) once they reached approximately 80% confluence. Cell Counting Kit-8 (CCK-8) assay was performed to evaluate the proliferation of LEC B3. The mRNA of Notch 3 was detected via RNA extraction and quantitative real-time PCR (RT-qPCR). The protein level of Notch 3 was measured by western blot.

Results: The mRNA and protein expression of Notch 3 were evidently down-regulated in H2O2-inducted LEC B3. Overexpression of Notch 3 increased the proliferation and suppressed the apoptosis of H2O2-inducted LECs B3. The elevated level of Notch 3 decreased the reactive oxygen species (ROS) fluorescence intensity and decreased Fe2+ and total Fe levels. In addition, Notch 3 up-regulation increased the levels of ferroptosis-related proteins GPX4 and SLC7A11. Notch 3 overexpression decreased the protein levels of p-PI3K, and p-AKT in H2O2-treated LECs B3. PI3K/AKT pathway inhibitor reversed the role effect of Notch 3 overexpression on the proliferation, apoptosis, and ferroptosis of LECs cells in ARC model.

Conclusion: The present study identified that Notch 3 regulates ferroptosis of LECs B3 in ARC by PI3K/AKT pathway, which might offer a novel biomarker for the future investigation of the target of ARC.

Purpose: To investigate the pathogenesis of type-2 macular telangiectasia (MacTel) by comparing the levels of glial fibrillary acidic protein (GFAP), aquaporin-4 (AQP4), and K+ inwardly rectifying channel 4.1 (Kir4.1) in the aqueous humor of diagnosed patients and individuals who had no ophthalmological disease.

Methods: This prospective study included nine patients with cataract and MacTel type 2 (group 1) and patients without any ophthalmological pathology other than senile cataract (group 2). We comparatively analyzed the groups' GFAP, AQP4, and Kir4.1 levels in the anterior chamber fluid, which was sampled intraoperatively during the cataract surgery.

Results: The GFAP levels were found to be 601.18 ± 66.19 pg/mL in the patient group and 1059 ± 537 pg/mL in the control group, and the difference was statistically significant. (P = 0.019) The mean AQP4 levels were lower (1.5 ± 1.02 ng/mL) in the patient group than in the control group (2.81 ± 1.19 pg/mL) (P = 0.012). There was no significant difference in terms of the mean Kir4.1 levels between the groups (P = 0.453). There was a significant negative correlation between the postoperative best corrected visual acuity (logMAR) and GFAP and AQP4 (for GFAP; r = -0.473 P = 0.02, for AQP4 r = -0.463 P = 0.023).

Discussion: GFAP and AQP4 levels may be related to glial cell dysfunction and disturbances in retinal fluid balance in the pathophysiology of MacTel type 2.

Purpose: Macrophage-like cells (MLCs) in the vitreoretinal interface are involved in angiogenesis and retinal homeostasis. This study investigated the changes in the MLCs at the vitreoretinal interface using optical coherence tomography angiography (OCTA) with progression of diabetic retinopathy (DR) and treatment response.

Methods: This cross-sectional, retrospective, observational study involved 86 eyes, categorized into four groups: Diabetes Mellitus without DR (n = 17), DME without treatment (n = 22), DME with anti-VEGF (n = 23), and DME with Dexamethasone (n = 24). The MLCs were imaged in the vitreoretinal interface slab 3 micron from the internal limiting membrane in OCTA. The images were processed with Image J and overlaid on the angiography en face image.

Results: Significant differences in MLC count ( P = 0.038), MLC density ( P = 0.007), and central subfield thickness (CST) ( P = 0.000) were observed with increasing severity and progression from no DR to DME. Both anti-VEGF and DEX treatment were associated with significant reduction in MLC count ( P = 0.000, 0.002), MLC density ( P = 0.000, 0.002), and CST ( P = 0.008, 0.030) A positive significant correlation was noted between MLC density and change in BCVA and CST. No significant difference was noted between anti-VEGF and DEX groups.

Conclusions: MLCs increase with worsening DR and show reduction with treatment response with direct correlation with BCVA and CST. MLCs can act as a surrogate marker for treatment response in DME.

Aviation ophthalmology is an unexplored branch of ophthalmology. This specialized field combines the principles of ophthalmology and aerospace medicine to ensure optimal visual performance and ocular health in aircrew for safer flights. The unique stressors encountered in flight, such as rapid acceleration, hypoxia, glare, and sudden changes in lighting, can significantly affect visual performance. Thus, ophthalmologic evaluation forms a critical component of medical fitness assessments for flying personnel. Given the visually demanding and high-risk environment of aviation, maintaining strict visual standards is crucial for flight safety. However, controversies still exist in the different governing bodies that are responsible for aviation visual requirements. This review article aims to present a comprehensive overview of the visual standards, common ophthalmic disorders affecting aviators, and controversies in aviation ophthalmology. It discusses in detail the visual tasks essential in flight-such as distance and near visual acuity, color perception, depth judgment, contrast sensitivity, and night vision-and the minimum standards set by regulatory authorities like the Directorate General of Civil Aviation (DGCA), Federal Aviation Administration (FAA), and others. It also highlights ocular diseases disposal in aviation.

Purpose: Corneal neovascularization (CNV) threatens corneal transparency and is a leading cause of vision loss. This study evaluates the anti-angiogenic effects of extracellular vesicles (EVs) derived from human corneal stromal stem cells (CSSCs).

Methods: Cultured human umbilical vein endothelial cells (HUVECs) were treated with CSSC-EVs to examine the influence on cell growth and modulation of angiogenesis using xCELLigence and tube formation assays. In vivo, a mouse model of CNV was induced by silver nitrate (AgNO₃) cauterization, and the injured corneas were treated with CSSC-EV eye drops twice daily for four days. On day 10, new vessel formation on mouse corneas was graded, and the expression of angiogenic markers was assessed using immunostaining and qPCR. Results were analyzed using one-way ANOVA.

Results: HUVEC cultures treated with CSSC-EVs showed reduced growth with a significant increase in cell doubling time. On Geltrex-coated culture surface, HUVECs incubated with CSSC-EVs generated reduced numbers of vascular tube structures, with significantly reduced junctions and nodes. In vivo, CNV developed in AgNO₃-cauterized mouse corneas by day 10 post-injury. Eye drop treatment with CSSC-EVs attenuated the formation of new vessels expressing vascular marker CD31 and lymphatic marker LYVE1. Compared to injured controls treated with phosphate-buffered saline (PBS) eye drops, the expression of angiogenic markers, including ANGPT1 and 2, CD31, VEGFA, VEGFR1, and R2, was significantly downregulated in EV-treated corneas (P < 0.05).

Conclusion: The anti-angiogenic effect of CSSC-EVs demonstrated their potential to inhibit CNV. Overall, the topical application of CSSC-EVs was safe and effective for addressing CNV-related pathologies.

Purpose: To compare the biochemical and histopathological effects of ramucirumab and bevacizumab in a streptozotocin (STZ)-induced experimental diabetic retinopathy (DR) rat model.

Methods: A total of 40 adult male Sprague-Dawley rats were divided into four groups: Control, STZ, STZ + bevacizumab (2.5 mg/kg, intraperitoneal, single dose), and STZ + ramucirumab (8 mg/kg, intraperitoneal, single dose). Oxidative stress and inflammatory markers, including superoxide dismutase (SOD), interleukin-1 beta (IL-1β), and transforming growth factor beta-1 (TGF-β1), as well as vascular endothelial growth factor-A (VEGF-A) levels, were measured using enzyme-linked immunosorbent assay. Histopathological evaluations were performed using hematoxylin-eosin, periodic acid-Schiff, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Statistical analyses were conducted using ANOVA and nonparametric tests (P < 0.05).

Results: STZ administration significantly increased VEGF-A and IL-1β levels while decreasing SOD levels. Both bevacizumab and ramucirumab significantly reduced VEGF-A and IL-1β levels and restored SOD values toward control levels. Histopathological analyses revealed that neovascularization, endothelial proliferation, basement membrane thickening, and vascular hyalinization observed in the STZ group were markedly reduced in the treatment groups. No significant difference in efficacy was detected between the bevacizumab and ramucirumab groups.

Conclusion: Ramucirumab provided biochemical and histopathological improvements comparable to bevacizumab in the experimental DR model. These findings suggest that ramucirumab may represent an alternative or complementary option to existing anti-VEGF therapies in ophthalmology. Furthermore, the results highlight the simultaneous role of angiogenesis, inflammation, and oxidative stress in the pathogenesis of DR. Larger, longer-term studies with different dosing protocols are warranted.

Purpose: Low-dose 650 nm red light has been found to slow myopia progression, although the underlying mechanisms remain unclear. This study aimed to investigate its antioxidative effects and molecular pathways.

Methods: An oxidative stress model was established in ARPE-19 cells by treatment with hydrogen peroxide (H₂O₂) at concentrations of 0, 0.5, and 0.75 mM. The cells were then irradiated with red light for 9 minutes, twice daily for 2 days, with an equivalent-power white light group serving as a control. Following irradiation, oxidative stress was quantified using a DCFH-DA assay, and DNA damage was assessed by γ-H2AX immunofluorescence. For the in vivo study, mice received ocular irradiation with red light (9 minutes/session, twice daily for 5 days) using a white light-exposed group as a control. Changes in axial length were measured post irradiation using anterior segment optical coherence tomography. Subsequently, retinal pigment epithelial (RPE) cells were isolated from the mice for RNA sequencing to analyze differential mRNA expression. Quantitative real-time PCR (qPCR) and Western blotting were employed to validate the expression of specific genes associated with ocular diseases.

Results: At a concentration of 0.75 mM hydrogen peroxide, red light irradiation significantly reduces oxidative stress levels compared to the control group. RNA sequencing data revealed that there were 274 genes upregulated and 225 genes downregulated in RPE cells from mouse eyes illuminated with the 650 nm red light. The gene encoding aldehyde dehydrogenase 3A1 (ALDH3A1), which is significantly upregulated after red light irradiation, plays an important role in protecting ocular structures from oxidative damage. qPCR and Western blot analyses confirmed that ALDH3A1 was heightened in RPE cells from mouse eyes in vivo and in cultured human RPE cells in vitro illuminated by the 650 nm red light.

Conclusions: ALDH3A1 may play a part in myopia improvement upon 650 nm red light illumination.