Simultaneous bilateral purtscher like retinopathy with systemic lupus erythematosus: a case.

BACKGROUD: Systemic lupus erythematosus is an unexplained autoimmune disease involving multiple systems throughout the body, and its ocular changes include dry eye, monocular or binocular visual field defects, vaso-occlusive diseases, or ischemic optic neuropathy. CASE PRESENTATION: This article reports a patient with SLE complicated with bilateral Purtscher like retinopathy, who had a sudden decrease in ocular vision as the first symptom, the autoantibodies related to phospholipid syndrome showed no abnormality, and both anti-dsDNA antibodies and anti-SM antibodies were significantly positive, indicating that anti-dsDNA antibodies and anti-SM antibodies were also important factors in the pathogenesis of Purtscher like retinopathy. CONCLUSION: The close relationship between SLE retinopathy and systemic inflammatory activities and emphasize the importance of systemic immunotherapy.

Purtscher's and Purtscher-like retinopathy etiology, features, management, and outcomes: A summative systematic review of 168 cases.

BACKGROUND: To describe Purtscher's and Purtscher-like retinopathy clinical features, etiologies, management options, and visual outcomes. METHODS: Our protocol was registered on PROSPERO [registration number: CRD42023406843]. Seven online databases were searched: PubMed, Scopus, Medline, ScienceDirect, CENTRAL, clinicaltrials.gov, and Google Scholar. Original articles were included if they reported at least one subject diagnosed with Purtscher's or Purtscher-like retinopathy. The primary outcome is to describe the clinical features of Purtscher and Purtscher-like retinopathies, including etiologies, results of related investigations, management lines, and visual outcomes. All analyses were conducted with the use of Statistical Package for Social Sciences (SPSS) version 27 (IBM SPSS Corp, SPSS Statistics ver. 26, USA) and Cochrane's RevMan software. The methodological quality of included studies was assessed using the NIH quality assessment tools. RESULTS: A total of 114 articles were included, describing 168 cases of Purtscher's and Purtscher-like retinopathy. Patients were evenly distributed between males (50.89%) and females (49.11%). Average age of patients was 34.62 years old. Trauma was the leading cause of retinopathy, being reported in 39.88% of our patients, followed by systemic lupus erythematosus (SLE) (13.1%) and acute pancreatitis (11.9%). Bilateral symptoms were reported in 57.7% of patients with centrally blurred vision being the most complained symptom (OS: 34.32% and OD: 18%). 75% of patients elicited bilateral retinal findings. Cotton-wool spots were of highest prevalence (58%). Purtscher flecken was seen in 53% of patients. Macular edema was seen in 13% of patients. Overall, patients had a favorable prognosis (53%). CONCLUSION: Purtscher's and Purtscher-like retinopathies are rare sight-threatening retinopathies that develop most commonly following trauma or other systemic diseases as SLE and acute pancreatitis. Little data is available regarding these conditions, and available data is of low quality. Patients develop bilateral disease in approximately 50% of cases, and several retinal findings are observed, with no specific tendency. Most observed signs are cotton-wool spots in around 55% of patients and Purtscher flecken in 51% of patients. Patients spontaneously recovered, although data is not conclusive. No clear prognostic value of etiological factors is identified, and further research is required in this regard.

Role of caspase-11 non-canonical inflammasomes in retinal ischemia/reperfusion injury.

BACKGROUND: Retinal ischemia/reperfusion (IR) injury is a common pathological process in many ophthalmic diseases. Interleukin-1ß (IL-1ß) is an important inflammatory factor involved in the pathology of retinal IR injury, but the mechanism by which IL-1ß is regulated in such injury remains unclear. Caspase-11 non-canonical inflammasomes can regulate the synthesis and secretion of IL-1ß, but its role in retinal IR injury has not been elucidated. This study aimed to evaluate the role of caspase-11 non-canonical inflammasomes in retinal IR injury. METHODS: Retinal IR injury was induced in C57BL/6J mice by increasing the intraocular pressure to 110 mmHg for 60 min. The post-injury changes in retinal morphology and function and in IL-1ß expression were compared between caspase-11 gene knockout (caspase-11-/-) mice and wild-type (WT) mice. Morphological and functional changes were evaluated using hematoxylin-eosin staining and retinal whole mount staining and using electroretinography (ERG), respectively. IL-1ß expression in the retina was measured using enzyme-linked immunosorbent assay (ELISA). The levels of caspase-11-related protein were measured using western blot analysis. The location of caspase-11 in the retina was determined via immunofluorescence staining. Mouse type I astrocytes C8-D1A cells were used to validate the effects of caspase-11 simulation via hypoxia in vitro. Small-interfering RNA targeting caspase-11 was constructed. Cell viability was evaluated using the MTT assay. IL-1ß expression in supernatant and cell lysate was measured using ELISA. The levels of caspase-11-related protein were measured using western blot analysis. RESULTS: Retinal ganglion cell death and retinal edema were more ameliorated, and the ERG b-wave amplitude was better after retinal IR injury in caspase-11-/- mice than in WT mice. Further, caspase-11-/- mice showed lower protein expressions of IL-1ß, cleaved caspase-1, and gasdermin D (GSDMD) in the retina after retinal IR injury. Caspase-11 protein was expressed in retinal glial cells, and caspase-11 knockdown played a protective role against hypoxia in C8-D1A cells. The expression levels of IL-1ß, cleaved caspase-1, and GSDMD were inhibited after hypoxia in the si-caspase-11 constructed cells. CONCLUSIONS: Retinal IR injury activates caspase-11 non-canonical inflammasomes in glial cells of the retina. This results in increased protein levels of GSDMD and IL-1ß and leads to damage in the inner layer of the retina.

[Vascularized foveal zone: prevalence and structural characteristics]. / Vaskulyarizovannaya foveal'naya zona: rasprostranennost' i strukturnye kharakteristiki.

PURPOSE: This study was performed to assess the prevalence of the vascularized foveal zone, including macular-foveal capillaries (MFC) and congenital retinal macrovessels (CRM), and to analyze the structural characteristics of the macular area in patients with MFC. MATERIAL AND METHODS: The first phase of the study evaluated the prevalence of MFC and CRM. Optical coherence tomography angiography (OCT-A) was performed, and OCT-A images of the foveal avascular zone were analyzed. In the second phase, two groups were formed: the MFC group (12 eyes, 9 patients, mean age 43.8±10.7 years) and the control group (18 eyes, 17 patients, mean age 43.0±11.8 years). A comparative analysis was performed assessing central retinal thickness (CRT), thickness of retinal nerve fiber layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), outer plexiform layer (OPL), outer nuclear layer (ONL), and foveal pit depth. RESULTS: MFCs were detected in 45 eyes from a total sample of 1031 eyes of 536 patients. The presence of CRM was recorded in three eyes of three patients. RNFL thickness was significantly higher in the MFC group in the inferior parafoveal sector (26.50 [26.00; 29.50] and 24.50 [21.75; 26.50] µm; p=0.022) and in the foveal zone (15.50 [14.00; 16.00] and 12.00 [11.00; 14.00] µm; p=0.017). Additionally, patients with MFC had a higher thickness of GCL and IPL in the fovea, inferior, nasal, and temporal parafoveal sectors. The depth of the foveal pit was significantly lower in the MFC group compared to the control group (83.0 [77.4; 101.6] and 128.0 [107.5; 147.05] µm; p=0.001). CONCLUSION: The prevalence of MFC was 4.36% (calculated per number of eyes), while the prevalence of CRM - 0.29%. The macular area in patients with MFC had increased thickness of the inner retinal layers and decreased depth of the foveal pit, suggesting potential disruption in the natural process of ganglion cell migration and apoptosis during embryogenesis.

Optical Coherence Tomography Angiography of Macular Microangiopathy in Children With Sickle Cell Disease.

In this study, we identified the presence of sickle cell maculopathy and determined correlations between hemolysis indicators and systemic and ocular manifestations in children with sickle cell disease (SCD). Thirty-three patients with SCD 5 to 18 years of age underwent optical coherence tomography angiography (OCTA) as part of a thorough eye examination. The hematological indices and clinical data (hemoglobin, fetal hemoglobin, mean corpuscular volume, and frequency of sickle cell-associated complications and therapy) were collected. The SCD group contained 33 patients (66 eyes), and the control group contained 36 healthy participants (72 eyes). The SCD group had significantly thinner parafoveal thickness ( P =0.041) and significantly smaller parafoveal volume ( P =0.041) than the controls. The SCD group had lower deep capillary plexus density than the controls ( P =0.029). The SCD group had significantly smaller flow areas than the controls ( P <0.001). The foveal avascular zone (FAZ) perimeter, foveal density, and FAZ area in the entire retina did not differ significantly between the groups ( P >0.05). The platelet level was negatively correlated with parafoveal and perifoveal thickness and density. OCTA detected early macular microvascular changes in children and adolescents with asymptomatic SCD.

Thrombotic Microangiopathy Following Hematopoietic Stem Cell Transplantation: A Case of Purtscher-like Retinopathy.

Purtscher-like retinopathy (PLR) is a rare entity related with retinal ischemia due to endothelial dysfunction and embolization. We present a case of a 17-year-old patient who presented with PLR associated with transplant-associated thrombotic microangiopathy. Visual acuity was finger counting at 1 meter in both eyes. Fundoscopy demonstrated peripapillary cotton-wool spots and hypopigmentation in the middle peripheral retina. Both eyes showed signs of macular edema with intraretinal hemorrhages. Optical coherence tomography and fundus fluorescence angiography was performed to support the diagnosis. After systemic treatments and panretinal photocoagulation, the patient's vision improved and the macular edema resolved. [Ophthalmic Surg Lasers Imaging Retina 2024;55:603-606.].

Effects of Acute High-Altitude Exposure on Morphology and Function of Retinal Ganglion Cell in Mice.

Purpose: High altitude retinopathy (HAR) is a retinal functional disorder caused by inadequate adaptation after exposure to high altitude. However, the cellular and molecular mechanisms underlying retinal dysfunction remain elusive. Retinal ganglion cell (RGC) injury is the most important pathological basis for most retinal and optic nerve diseases. Studies focusing on RGC injury after high-altitude exposure (HAE) are scanty. Therefore, the present study sought to explore both functional and morphological alterations of RGCs after HAE. Methods: A mouse model of acute hypobaric hypoxia was established by mimicking the conditions of a high altitude of 5000 m. After HAE for 2, 4, 6, 10, 24, and 72 hours, the functional and morphological alterations of RGCs were assessed using retinal hematoxylin and eosin (H&E) sections, retinal whole mounts, transmission electron microscopy (TEM), and the photopic negative response (PhNR) of the electroretinogram. Results: Compared with the control group, the thickness of the ganglion cell layer and retinal nerve fiber layer increased significantly, RGC loss remained significant, and the amplitudes of a-wave, b-wave, and PhNR were significantly reduced after HAE. In addition, RGCs and their axons exhibited an abnormal ultrastructure after HAE, including nuclear membrane abnormalities, uneven distribution of chromatin in the nucleus, decreased cytoplasmic electron density, widening and vacuolization of the gap between axons, loosening and disorder of myelin sheath structure, widening of the gap between myelin sheath and axon membrane, decreased axoplasmic density, unclear microtubule and nerve fiber structure, and abnormal mitochondrial structure (mostly swollen, with widened membrane gaps and reduced cristae and vacuolization). Conclusions: The study findings confirm that the morphology and function of RGCs are damaged after HAE. These findings lay the foundation for further study of the specific molecular mechanisms of HAR and promote the effective prevention.

Ocular fundus changes and association with systemic conditions in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease that affects multiple organs and systems. Ocular involvement is estimated to manifest in one-third of individuals with SLE, of which lupus retinopathy and choroidopathy represent the severe subtype accompanied by vision impairment. Advancements in multimodal ophthalmic imaging have allowed ophthalmologists to reveal subclinical microvascular and structural changes in fundus of patients with SLE without ocular manifestations. Both ocular manifestations and subclinical fundus damage have been shown to correlate with SLE disease activity and, in some patients, even precede other systemic injuries as the first presentation of SLE. Moreover, ocular fundus might serve as a window into the state of systemic vasculitis in patients with SLE. Given the similarities of the anatomy, physiological and pathological processes shared among ocular fundus, and other vital organ damage in SLE, such as kidney and brain, it is assumed that ocular fundus involvement has implications in the diagnosis and evaluation of other systemic impairments. Therefore, evaluating the fundus characteristics of patients with SLE not only contributes to the early diagnosis and intervention of potential vision damage, but also holds considerate significance for the evaluation of SLE vasculitis state and prediction of other systemic injuries.

Optimization of an Ischemic Retinopathy Mouse Model and the Consequences of Hypoxia in a Time-Dependent Manner.

The retina is one of the highest metabolically active tissues with a high oxygen consumption, so insufficient blood supply leads to visual impairment. The incidence of related conditions is increasing; however, no effective treatment without side effects is available. Furthermore, the pathomechanism of these diseases is not fully understood. Our aim was to develop an optimal ischemic retinopathy mouse model to investigate the retinal damage in a time-dependent manner. Retinal ischemia was induced by bilateral common carotid artery occlusion (BCCAO) for 10, 13, 15 or 20 min, or by right permanent unilateral common carotid artery occlusion (UCCAO). Optical coherence tomography was used to follow the changes in retinal thickness 3, 7, 14, 21 and 28 days after surgery. The number of ganglion cells was evaluated in the central and peripheral regions on whole-mount retina preparations. Expression of glial fibrillary acidic protein (GFAP) was analyzed with immunohistochemistry and Western blot. Retinal degeneration and ganglion cell loss was observed in multiple groups. Our results suggest that the 20 min BCCAO is a good model to investigate the consequences of ischemia and reperfusion in the retina in a time-dependent manner, while the UCCAO causes more severe damage in a short time, so it can be used for testing new drugs.

Retinal light damage: From mechanisms to protective strategies.

Visible light serves as a crucial medium for vision formation.;however, prolonged or excessive exposure to light is recognized as a significant etiological factor contributing to retinal degenerative diseases. The retina, with its unique structure and adaptability, relies on the homeostasis of cellular functions to maintain visual health. Under normal conditions, the retina can mount adaptive responses to various insults, including light-induced damage. Unfortunately, exposure to intense and excessive light triggers a cascade of pathological alterations in retinal photoreceptor cells, pigment epithelial cells, ganglion cells, and glial cells. These alterations encompass disruption of intracellular REDOX and Ca²âº homeostasis, pyroptosis, endoplasmic reticulum stress, autophagy, and the release of inflammatory cytokines, culminating in irreversible retinal damage. We first delineate the mechanisms of retinal light damage through 4 main avenues: mitochondria function, endoplasmic reticulum stress, cell autophagy, and inflammation. Subsequently, we discuss protective strategies against retinal light damage, aiming to guide research toward the prevention and treatment of light-induced retinal conditions.

Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury.

Ischemia-induced retinopathy is a hallmark finding of common visual disorders including diabetic retinopathy (DR) and central retinal artery and vein occlusions. Treatments for ischemic retinopathies fail to improve clinical outcomes and the design of new therapies will depend on understanding the underlying disease mechanisms. Histone deacetylases (HDACs) are an enzyme class that removes acetyl groups from histone and non-histone proteins, thereby regulating gene expression and protein function. HDACs have been implicated in retinal neurovascular injury in preclinical studies in which nonspecific HDAC inhibitors mitigated retinal injury. Histone deacetylase 3 (HDAC3) is a class I histone deacetylase isoform that plays a central role in the macrophage inflammatory response. We recently reported that myeloid cells upregulate HDAC3 in a mouse model of retinal ischemia-reperfusion (IR) injury. However, whether this cellular event is an essential contributor to retinal IR injury is unknown. In this study, we explored the role of myeloid HDAC3 in ischemia-induced retinal neurovascular injury by subjecting myeloid-specific HDAC3 knockout (M-HDAC3 KO) and floxed control mice to retinal IR. The M-HDAC3 KO mice were protected from retinal IR injury as shown by the preservation of inner retinal neurons, vascular integrity, and retinal thickness. Electroretinography confirmed that this neurovascular protection translated to improved retinal function. The retinas of M-HDAC3 KO mice also showed less proliferation and infiltration of myeloid cells after injury. Interestingly, myeloid cells lacking HDAC3 more avidly engulfed apoptotic cells in vitro and after retinal IR injury in vivo compared to wild-type myeloid cells, suggesting that HDAC3 hinders the reparative phagocytosis of dead cells, a process known as efferocytosis. Further mechanistic studies indicated that although HDAC3 KO macrophages upregulate the reparative enzyme arginase 1 (A1) that enhances efferocytosis, the inhibitory effect of HDAC3 on efferocytosis is not solely dependent on A1. Finally, treatment of wild-type mice with the HDAC3 inhibitor RGFP966 ameliorated the retinal neurodegeneration and thinning caused by IR injury. Collectively, our data show that HDAC3 deletion enhances macrophage-mediated efferocytosis and protects against retinal IR injury, suggesting that inhibiting myeloid HDAC3 holds promise as a novel therapeutic strategy for preserving retinal integrity after ischemic insult.

Advances in sickle cell retinopathy screening techniques, tests, and practices: A systematic review.

Sickle cell retinopathy (SCR) is a progressive, sight-threatening ophthalmic complication of sickle cell disease (SCD). Current SCR screening focuses on the detection of pathologic sea fan neovascularization, the first sign of proliferative sickle cell retinopathy (PSR). If untreated, PSR can lead to severe visual impairment and blindness through progression to vitreous hemorrhage and/or retinal detachment. SCR screening with dilated fundus examination (DFE) is recommended every 1-2 years starting at age 10, but data underlying this recommendation are of poor quality and based upon expert consensus. We performed a systematic review to characterize imaging techniques, laboratory-based tests, and clinical practices for SCR screening. This PROSPERO-registered systematic review included relevant texts identified through predetermined searches in online databases. Collected test accuracy data facilitated the calculation of likelihood ratios. Forty-four studies evaluating 4928 patients were included. DFE demonstrated moderate test accuracy (LR+ of 8.0, LR- of 0.3). Ultra-widefield-fundus photography demonstrated superior accuracy (LR+ 32.5, LR- 0.03). Optical coherence tomography angiography applications were highly accurate for PSR identification (machine learning LR+ 32.5, LR- 0.03; human grader LR+ 2.8-213.1, LR- 0.1-0.2). Most techniques and tests were more accurate at detecting PSR than staging SCR or detecting lower-grade SCR. Our findings support the integration of advanced image-based approaches, such as computer-based image analysis and ultra-wide-field fundus imaging, for SCR screening in SCD patients given the superior accuracy in PSR detection compared with the current standard of care. Rigorous SCR screening implementation studies are needed to support evidence-based SCR screening recommendations.

Optical coherence tomography characteristics and prognostic predictors of acute macular neuroretinopathy following SARS-CoV-2 infection.

PURPOSE: To analyze the characteristics of optical coherence tomography in acute macular neuroretinopathy (AMN) following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and discuss the prognostic predictors. METHODS: Patients with AMN following SARS-CoV-2 infection were divided into two groups according to the presence or absence of hyperreflective outer nuclear layer (ONL) lesion involving the fovea. RESULTS: The first visit included 14 eyes in the fovea-involved group and 20 eyes in the no fovea-involved group. Ellipsoid zone (EZ) hyporeflection and interdigitation zone (IZ) interruption were detected in all eyes. Other common manifestations were myoid zone (MZ) hyperreflection (76.5%), ONL hyperreflection (73.5%), outer plexiform layer (OPL) thickening (64.7%), and EZ interruption (50%). The follow-up period was 48.4 ± 55.3 days. At the last visit, 12 eyes were in the fovea-involved group and 13 eyes in the no fovea-involved group. IZ interruption was detected in all eyes. Other common manifestations were EZ hyporeflection (92.0%), ONL atrophy (40.0%), OPL thickening (36.0%), OPL linear (32.0%), and MZ hyperreflection (32%). The improvement of visual acuity (VA) was -0.5 ± 0.5 and -0.2 ± 0.4 in the fovea-involved group and the no fovea-involved group, respectively, with a statistically significant difference between them (P = 0.045). Initial VA, initial cotton wool spot, initial ONL cyst, final ONL cyst, and final OPL linear were associated with final VA (P = 0.000, P = 0.029, P = 0.044, P = 0.049, P = 0.049, respectively). CONCLUSIONS: In the early stage of AMN following SARS-CoV-2 infection, IZ interruption and EZ hyporeflection were the most common manifestations, and pathology of IZ was more serious than that of EZ. Subsequently, OPL and ONL atrophied, and ONL atrophied faster. Regardless of whether hyperreflective ONL involved the fovea, VA improved, with a more noticeable improvement found in the fovea-involved group. The presence of initial ONL cyst and initial cotton wool spot, rapid atrophy of OPL, and poorer initial VA indicating poorer VA outcome.

Multimodal Analysis of the Retinal Manifestations of Tuberous Sclerosis Complex: A Case Series.

BACKGROUND AND OBJECTIVE: We used a multi-modal imaging approach including fundus fluorescein angiography (FFA) to assess the retinal lesions in tuberous sclerosis complex (TSC) and evaluate their correlation with intracranial tuber burden on magnetic resonance imaging (MRI). PATIENTS AND METHODS: Participants with TSC underwent bilateral fundus photography, optical coherence tomography (OCT), infrared (IR) imaging, and FFA. Participants' most recent MRI brain scans were analyzed to determine intracranial tuber load. RESULTS: Nine participants were included. OCT identified all retinal astrocytic hamartoma (RAH) lesions, IR identified 75%, fundus photography identified 63%, and FFA detected just 57%. On FFA, 20% of flat-type hamartomas and all multi-nodular and transitional types were hyperfluorescent. There were significant positive correlations between the quantities of intracranial tubers and all TSC-retinal lesions (r = 0.8, P < 0.01) and all RAH lesions (r = 0.8, P = 0.01). CONCLUSIONS: A multimodal imaging-based approach with fundal photography, IR imaging, and OCT should be used to assess the retina in TSC as it may indicate the intracranial tuber burden. [Ophthalmic Surg Lasers Imaging Retina 2024;55:568-574.].

Retinal integrity in human babesiosis: a pilot study.

BACKGROUND: Prior case reports and animal studies have reported on potential ophthalmologic complications of babesiosis, but this issue has not previously been addressed in a cohort of patients with babesiosis. This cross-sectional descriptive pilot study evaluated the retinas of patients with acute babesiosis to determine if retinal abnormalities are a feature of the disease. METHODS: We screened all patients admitted to Yale New Haven Hospital with laboratory confirmed babesiosis during the summer of 2023 and obtained informed consent. Patients were interviewed and underwent pupil dilation and a retinal examination using an indirect ophthalmoscope. Demographic and clinical information were obtained by questionnaire and through chart review. RESULTS: Ten patients underwent retinal eye exams with results that were generally unremarkable. No study patients showed any signs of retinal inflammation, infection, retinal bleeding, retinal tears, or abnormal vessel formation that could be attributed to infection. CONCLUSION: This small study did not find evidence of retinopathy in patients with babesiosis. Further studies with larger populations, repeated exams, and long term follow up will further elucidate the potential small vessel complications of human babesiosis.

Choroidal thinning in myopia is associated with axial elongation and severity of myopic maculopathy.

High myopia can lead to pathologic myopia and visual impairment, whereas its causes are unclear. We retrospectively researched high myopia cases from patient records to investigate the association between axial elongation and myopic maculopathy. Sixty-four eyes were examined in patients who visited the department between July 2017 and June 2018, had an axial length of 26 mm or more, underwent fundus photography, and had their axial length measured twice or more. The average axial length was 28.29 ± 1.69 mm (mean ± standard deviation). The average age was 58.3 ± 14.4 years old. Myopic maculopathy was categorized as mild (grades 0 and 1) and severe (grades 2, 3, and 4). The severe group had longer axial lengths than the mild group (P < 0.05). Moreover, the severe group exhibited thinner choroidal thickness than the mild group (P < 0.05). When subjects were grouped by axial elongation over median value within a year, the elongation group showed thinner central choroidal thickness than the non-elongation group (142.1 ± 91.9 vs. 82.9 ± 69.8, P < 0.05). In conclusion, in patients with high myopia, the severity of maculopathy correlated with choroidal thickness and axial length. Thinner choroidal thickness was associated with axial elongation based on the baseline axial length.

Protective effect and mechanism of Lycium ruthenicum Murray anthocyanins against retinal damage induced by blue light exposure.

Lycium ruthenicum Murray (LR) is a medicine and edible plant in Northwest China, and L. ruthenicum Murray anthocyanins (LRA) are green antioxidants with various pharmacological activities, such as antioxidant and anti-inflammatory activities. However, the protective effect and mechanism of LRA against retinal damage induced by blue light exposure are poorly understood. This study explored the protective effects and potential mechanisms of LRA on retinal damage induced by blue light exposure in vitro and in vivo. The results showed that LRA could ameliorate oxidative stress injury by activating the antioxidant stress nuclear factor-related factor 2 pathway, promoting the expression of phase II detoxification enzymes (HO-1, NQO1) and endogenous antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), and reducing reactive oxygen species and malondialdehyde levels. Additionally, LRA could inhibit inflammatory response by decreasing the expression of blue light exposure-induced nuclear factor-κB (NF-κB) pathway-related proteins (NF-κB and p-IκBα), as well as interleukin (IL)-6, tumor necrosis factor-α, IL-1ß pro-inflammatory factors and pro-inflammatory chemokine VEGF, and increasing the expression of anti-inflammatory factor IL-10. Furthermore, LRA could ameliorate oxidative stress-induced apoptosis by upregulating Bcl-2 and downregulating Bax and Caspase-3 protein expression. All these results indicate that LRA can be used as an antioxidant dietary supplement for the treatment or prevention of retinal diseases.