Interleukin-17A in diabetic retinopathy: The crosstalk of inflammation and angiogenesis.

Diabetic retinopathy (DR) is a severe ocular complication of diabetes which can leads to irreversible vision loss in its late-stage. Chronic inflammation results from long-term hyperglycemia contributes to the pathogenesis and progression of DR. In recent years, the interleukin-17 (IL-17) family have attracted the interest of researchers. IL-17A is the most widely explored cytokine in IL-17 family, involved in various acute and chronic inflammatory diseases. Growing body of evidence indicate the role of IL-17A in the pathogenesis of DR. However, the pro-inflammatory and pro-angiogenic effect of IL-17A in DR have not hitherto been reviewed. Gaining an understanding of the pro-inflammatory role of IL-17A, and how IL-17A control/impact angiogenesis pathways in the eye will deepen our understanding of how IL-17A contributes to DR pathogenesis. Herein, we aimed to thoroughly review the pro-inflammatory role of IL-17A in DR, with focus in how IL-17A impact inflammation and angiogenesis crosstalk.

Trends in the global burden of vision loss among the older adults from 1990 to 2019.

Purpose: To quantify the global impact of vision impairment in individuals aged 65 years and older between 1990 and 2019, segmented by disease, age, and sociodemographic index (SDI). Methods: Using the Global Burden of Diseases 2019 (GBD 2019) dataset, a retrospective demographic evaluation was undertaken to ascertain the magnitude of vision loss over this period. Metrics evaluated included case numbers, prevalence rates per 100,000 individuals, and shifts in prevalence rates via average annual percentage changes (AAPCs) and years lived with disability (YLDs). Results: From 1990 to 2019, vision impairment rates for individuals aged 65 years and older increased from 40,027.0 (95% UI: 32,232.9-49,945.1) to 40,965.8 (95% UI: 32,911-51,358.3, AAPC: 0.11). YLDs associated with vision loss saw a significant decrease, moving from 1713.5 (95% UI: 1216.2-2339.7) to 1579.1 (95% UI: 1108.3-2168.9, AAPC: -0.12). Gender-based evaluation showed males had lower global prevalence and YLD rates compared to females. Cataracts and near vision impairment were the major factors, raising prevalence by 6.95 and 2.11%, respectively. Cataract prevalence in high-middle SDI regions and near vision deficits in high SDI regions significantly influenced YLDs variation between 1990 and 2019. Conclusion: Over the past three decades, there has been a significant decrease in the vision impairment burden in individuals aged 65 and older worldwide. However, disparities continue, based on disease type, regional SDI, and age brackets. Enhancing eye care services, both in scope and quality, is crucial for reducing the global vision impairment burden among the older adults.

Integrative metabolome and lipidome analyses of plasma in neovascular macular degeneration.

Age-related macular degeneration (AMD) causes irreversible vision-loss among the elderly in industrial countries. Neovascular AMD (nAMD), which refers to late-stage AMD, is characterized by severe vision-threatening choroidal neovascularization (CNV). Herein, we constructed a global metabolic network of nAMD, based on untargeted metabolomic and lipidomic analysis of plasma samples collected from sixty subjects (30 nAMD patients and 30 age-matched controls). Among the nAMD and control groups, 62 and 44 significantly different metabolites were detected in the positive and negative ion modes, respectively. Grouping analysis further showed that lipid and lipid-like molecule-based superclasses contained the highest number of significantly different metabolites. Lipidomic analysis revealed that 53 lipids among the nAMD and control groups differed significantly; these belonged to four major lipid categories (glycerophospholipids, sphingolipids, glycerolipids, and fatty acids). A discriminative biomarker panel comprising 16 metabolites and lipids, which was constructed using multivariate statistical machine learning methods, could effectively identify nAMD cases. Among these 16 compounds, eight were lipids that belonged to three lipid categories (glycerophospholipids, sphingolipids, and prenol lipids). The top three biomarkers with the highest importance scores were all lipids (a glycerophospholipid and two sphingolipids), highlighting the crucial role played by glycerophospholipid and sphingolipid pathways in nAMD. These differences between the metabolic and lipid profiles of nAMD patients and elderly individuals without AMD provide a readout of the overall metabolic status of nAMD. Further insights into the identified discriminative biomarkers may pave the way for future diagnostic and therapeutic interventions for nAMD.

Intravitreal injections with anti-VEGF agent aflibercept versus subthreshold micropulse laser for chronic central serous chorioretinopathy: the alternative treatment regimens for verteporfin-shortage in China.

PURPOSE: To compare short-term anatomical outcomes observed in optical coherence tomography (OCT) between intravitreal injection (IVI) with anti-vascular endothelial growth factor (VEGF) agent aflibercept (IVA) and subthreshold micropulse laser (SML) therapy in chronic central serous chorioretinopathy (cCSC). METHODS: Thirty-nine eyes of 36 patients with symptomatic cCSC in this retrospective study received either IVA or SML between December 2020 and August 2022. Spectral-domain-OCT (SD-OCT) findings were compared between the two treatment groups in terms of central macular thickness (CMT), serous subretinal fluid (SRF) height, the presence of pigment epithelial detachment (PED) and subretinal hyperreflective foci (HF) at baseline and one-month follow-up visits. RESULTS: Both groups showed significant reductions in CMT and SRF at one-month follow-up visit. However, there were no statistically significant differences between the IVA and SML groups. Complete SRF resolution was observed in 10 out of 21 and 7 out of 18 eyes in the IVA and SML groups, respectively; however, retinal pigment epithelial (RPE) damage remained persistent in patients with PEDs at baseline. CONCLUSIONS: Both IVA and SML were effective in treating cCSC. IVA and SML treatments had comparable effects in reducing CMT and SRF in eyes with cCSC. Further prospective studies with larger sample sizes and long-term follow-up visits are warranted to identify the long-term efficacy.

cCSC lead to subsequent irreversible photoreceptor damage and visual complaints.IVA and SML treatments have comparable effects in reducing CMT and SRF in cCSC eyes.

Altered oxylipin levels in human vitreous indicate imbalance in pro-/anti-inflammatory homeostasis in proliferative diabetic retinopathy.

Proliferative diabetic retinopathy (PDR) is an advanced stage of diabetic retinopathy (DR), characterized by retinal neovascularization. It is a progressive fundus disease and a severe complication of diabetes that causes vision impairment. Hyperglycemia-induced persistent low-grade inflammation is a crucial factor underlying the pathogenesis of DR-associated damage and contributing to the progression of PDR. Highly enriched polyunsaturated fatty acids (PUFAs) in the retina are precursors to oxidized metabolites, namely, oxylipins, which exert pro-inflammatory or anti-inflammatory (resolving) effects under different pathological conditions and have been implicated in diabetes. To evaluate differences in oxylipin levels in the vitreous obtained from PDR and non-diabetic subjects, we performed a targeted assessment of oxylipins. A total of 41 patients with PDR and 22 non-diabetic control subjects were enrolled in this study. Vitreous humor obtained during routinely scheduled vitrectomy underwent a targeted but unbiased screening for oxylipins using mass spectrometry-based lipidomics. We found 21 oxylipins showing statistically significant differences in their levels between PDR and non-diabetic subjects (p < 0.05). Lipoxygenase (LOX)- and cytochrome P450 (CYP)- derived oxylipins were the most affected, while cyclooxygenase (COX) oxylipins were affected to a lesser extent. When categorized by their precursor PUFAs, ±19,20-EpDPE, a CYP product of docosahexaenoic acid (DHA) and 12S-HETE, a LOX product of arachidonic acid (ARA), were increased by the largest magnitude. Moreover, of these 21 oxylipins, 7 were considered as potential biomarkers for discriminating PDR patients from the non-diabetic controls. Our results indicate that altered oxylipin levels in the vitreous implicate an underlying imbalanced inflammation-resolution homeostasis in PDR.

Establishing the ground squirrel as a superb model for retinal ganglion cell disorders and optic neuropathies.

Retinal ganglion cell (RGC) death occurs after optic nerve injury due to acute trauma or chronic degenerative conditions such as optic neuropathies (e.g., glaucoma). Currently, there are no effective therapies to prevent permanent vision loss resulting from RGC death, underlining the need for research on the pathogenesis of RGC disorders. Modeling human RGC/optic nerve diseases in non-human primates is ideal because of their similarity to humans, but has practical limitations including high cost and ethical considerations. In addition, many retinal degenerative disorders are age-related making the study in primate models prohibitively slow. For these reasons, mice and rats are commonly used to model RGC injuries. However, as nocturnal mammals, these rodents have retinal structures that differ from primates - possessing less than one-tenth of the RGCs found in the primate retina. Here we report the diurnal thirteen-lined ground squirrel (TLGS) as an alternative model. Compared to other rodent models, the number and distribution of RGCs in the TLGS retina are closer to primates. The TLGS retina possesses ~600,000 RGCs with the highest density along the equatorial retina matching the location of the highest cone density (visual streak). TLGS and primate retinas also share a similar interlocking pattern between RGC axons and astrocyte processes in the retina nerve fiber layer (RNFL). In addition, using TLGS we establish a new partial optic nerve injury model that precisely controls the extent of injury while sparing a portion of the retina as an ideal internal control for investigating the pathophysiology of axon degeneration and RGC death. Moreover, in vivo optical coherence tomography (OCT) imaging and ex vivo microscopic examinations of the retina in optic nerve injured TLGS confirm RGC loss precedes proximal axon degeneration, recapitulating human pathology. Thus, the TLGS retina is an excellent model, for translational research in neurodegeneration and therapeutic neuroprotection.

Iron Accumulation and Lipid Peroxidation in the Aging Retina: Implication of Ferroptosis in Age-Related Macular Degeneration.

Iron is an essential component in many biological processes in the human body. It is critical for the visual phototransduction cascade in the retina. However, excess iron can be toxic. Iron accumulation and reduced efficiency of intracellular antioxidative defense systems predispose the aging retina to oxidative stress-induced cell death. Age-related macular degeneration (AMD) is characterized by retinal iron accumulation and lipid peroxidation. The mechanisms underlying AMD include oxidative stress-mediated death of retinal pigment epithelium (RPE) cells and subsequent death of retinal photoreceptors. Understanding the mechanism of the disruption of iron and redox homeostasis in the aging retina and AMD is crucial to decipher these mechanisms of cell death and AMD pathogenesis. The mechanisms of retinal cell death in AMD are an area of active investigation; previous studies have proposed several types of cell death as major mechanisms. Ferroptosis, a newly discovered programmed cell death pathway, has been associated with the pathogenesis of several neurodegenerative diseases. Ferroptosis is initiated by lipid peroxidation and is characterized by iron-dependent accumulation. In this review, we provide an overview of the mechanisms of iron accumulation and lipid peroxidation in the aging retina and AMD, with an emphasis on ferroptosis.

Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush.

Purpose: To investigate the possible role of activating transcription factor 3 (ATF3) in retinal ganglion cell (RGC) neuroprotection and optic nerve regeneration after optic nerve crush (ONC). Methods: Overexpression of proteins of interest (ATF3, phosphatase and tensin homolog [PTEN], placental alkaline phosphatase, green fluorescent protein) in the retina was achieved by intravitreal injections of recombinant adenovirus-associated viruses (rAAVs) expressing corresponding proteins. The number of RGCs and αRGCs was evaluated by immunostaining retinal sections and whole-mount retinas with antibodies against RNA binding protein with multiple splicing (RBPMS) and osteopontin, respectively. Axonal regeneration was assessed via fluorophore-coupled cholera toxin subunit B labeling. RGC function was evaluated by recording positive scotopic threshold response. Results: The level of ATF3 is preferentially elevated in osteopontin+/RBPMS+ αRGCs following ONC. Overexpression of ATF3 by intravitreal injection of rAAV 2 weeks before ONC promoted RBPMS+ RGC survival and preserved RGC function as assessed by positive scotopic threshold response recordings 2 weeks after ONC. However, overexpression of ATF3 and simultaneous downregulation of PTEN, a negative regulator of the mTOR pathway, combined with ONC, only moderately promoted short distance RGC axon regeneration (200 µm from the lesion site) but did not provide additional RGC neuroprotection compared with PTEN downregulation alone. Conclusions: These results reveal a neuroprotective effect of ATF3 in the retina following injury and identify ATF3 as a promising agent for potential treatments of optic neuropathies.

Identification of altered microRNAs in retinas of mice with oxygen-induced retinopathy.

AIM: To identify disease-related miRNAs in retinas of mice with oxygen-induced retinopathy (OIR), and to explore their potential roles in retinal pathological neovascularization. METHODS: The retinal miRNA expression profile in mice with OIR and room air controls at postnatal day 17 (P17) were determined through miRNA microarray analysis. Several miRNAs were significantly up- and down-regulated in retinas of mice with OIR compared to controls by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Two databases including Targetscan7.1 and MirdbV5 were used to predict target genes that associated with those significantly altered miRNAs in retinas of mice with OIR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were also conducted to identify possible biological functions of the target genes. RESULTS: In comparison with room air controls, 3 and 8 miRNAs were significantly up- and down-regulated, respectively, in retinas of mice with OIR. The qRT-PCR data confirmed that mmu-miR-350-3p and mmu-miR-202-3p were significantly up-regulated, while mmu-miR-711 and mmu-miR-30c-1-3p were significantly down-regulated in mice with OIR compared to controls. GO analysis demonstrated that the identified target genes were related to functions such as cellular macromolecule metabolic process. KEGG pathway analysis showed a group of pathways, such as Wnt signaling pathway, transcriptional misregulation in cancer, Mucin type O-glycan biosynthesis, and mitogen-activated protein kinase (MAPK) signaling pathway might be involved in pathological process of retinal neovascularization. CONCLUSION: Our findings suggest that the differentially expressed miRNAs in retinas of mice with OIR might provide potential therapeutic targets for treating retinal neovascularization.

Imaging Kayser-Fleischer Ring in Wilson Disease Using In Vivo Confocal Microscopy.

PURPOSE: This study analyzes images of Kayser-Fleischer (K-F) rings in patients with Wilson disease (WD) using in vivo confocal microscopy (IVCM) and explores whether IVCM can be a useful clinical tool in facilitating the diagnosis and characterization of K-F rings. METHODS: One hundred four eyes of 52 patients with WD and K-F rings (K-F group) and 52 normal eyes of 52 age- and gender-matched control subjects (control group) were enrolled in the study. Both K-F and control groups consisted of 29 male patients and 23 female patients. IVCM imaging was performed, and images of the peripheral Descemet membrane were analyzed. RESULTS: All patients in K-F group showed abnormal patterns in the peripheral Descemet membrane from IVCM images. These abnormalities can be generally divided into 3 types: patchy, stripy, and spotty patterns. Each patient may have a combination of these patterns, with patchy pattern being most prevalent (100%), whereas stripy and spotty patterns are present in 30% to 40% of the K-F rings. Notably, these patterns are not correlated with other systematic symptoms of WD. CONCLUSIONS: IVCM images can be used as an objective clinical diagnostic tool to facilitate the identification of K-F rings and the diagnosis of WD.

iPSCs from a Hibernator Provide a Platform for Studying Cold Adaptation and Its Potential Medical Applications.

Hibernating mammals survive hypothermia (<10°C) without injury, a remarkable feat of cellular preservation that bears significance for potential medical applications. However, mechanisms imparting cold resistance, such as cytoskeleton stability, remain elusive. Using the first iPSC line from a hibernating mammal (13-lined ground squirrel), we uncovered cellular pathways critical for cold tolerance. Comparison between human and ground squirrel iPSC-derived neurons revealed differential mitochondrial and protein quality control responses to cold. In human iPSC-neurons, cold triggered mitochondrial stress, resulting in reactive oxygen species overproduction and lysosomal membrane permeabilization, contributing to microtubule destruction. Manipulations of these pathways endowed microtubule cold stability upon human iPSC-neurons and rat (a non-hibernator) retina, preserving its light responsiveness after prolonged cold exposure. Furthermore, these treatments significantly improved microtubule integrity in cold-stored kidneys, demonstrating the potential for prolonging shelf-life of organ transplants. Thus, ground squirrel iPSCs offer a unique platform for bringing cold-adaptive strategies from hibernators to humans in clinical applications. VIDEO ABSTRACT.

Retinal Astrocytes and GABAergic Wide-Field Amacrine Cells Express PDGFRα: Connection to Retinal Ganglion Cell Neuroprotection by PDGF-AA.

Purpose: Our previous experiments demonstrated that intravitreal injection of platelet-derived growth factor-AA (PDGF-AA) provides retinal ganglion cell (RGC) neuroprotection in a rodent model of glaucoma. Here we used PDGFRα-enhanced green fluorescent protein (EGFP) mice to identify retinal cells that may be essential for RGC protection by PDGF-AA. Methods: PDGFRα-EGFP mice expressing nuclear-targeted EGFP under the control of the PDGFRα promoter were used. Localization of PDGFRα in the neural retina was investigated by confocal imaging of EGFP fluorescence and immunofluorescent labeling with a panel of antibodies recognizing different retinal cell types. Primary cultures of mouse RGCs were produced by immunopanning. Neurobiotin injection of amacrine cells in a flat-mounted retina was used for the identification of EGFP-positive amacrine cells in the inner nuclear layer. Results: In the mouse neural retina, PDGFRα was preferentially localized in the ganglion cell and inner nuclear layers. Immunostaining of the retina demonstrated that astrocytes in the ganglion cell layer and a subpopulation of amacrine cells in the inner nuclear layer express PDGFRα, whereas RGCs (in vivo or in vitro) did not. PDGFRα-positive amacrine cells are likely to be Type 45 gamma-aminobutyric acidergic (GABAergic) wide-field amacrine cells. Conclusions: These data indicate that the neuroprotective effect of PDGF-AA in a rodent model of glaucoma could be mediated by astrocytes and/or a subpopulation of amacrine cells. We suggest that after intravitreal injection of PDGF-AA, these cells secrete factors protecting RGCs.

First report of CTNS mutations in a Chinese family with infantile cystinosis.

Infantile cystinosis (IC) is a rare autosomal recessive disorder characterized by a defect in the lysosomal-membrane transport protein, cystinosin. It serves as a prototype for lysosomal transport disorders. To date, several CTNS mutations have been identified as the cause of the prototypic disease across different ethnic populations worldwide. However, in Asia, the CTNS mutation is very rarely reported. For the Chinese population, no literature on CTNS mutation screening for IC is available to date. In this paper, by using the whole exome sequencing and Sanger sequencing, we identified two novel CTNS splicing deletions in a Chinese IC family, one at the donor site of exon 6 of CTNS (IVS6+1, del G) and the other at the acceptor site of exon 8 (IVS8-1, del GT). These data give information for the genetic counseling of the IC that occurred in Chinese population.

Rosiglitazone attenuates activation of human Tenon's fibroblasts induced by transforming growth factor-ß1.

PURPOSE: To investigate the influence of rosiglitazone on activation of human Tenon's fibroblasts (HTFs) and to access the possible mechanism. METHODS: Cultured human Tenon's fibroblasts were pretreated in two different concentrations of rosiglitazone (5 µmol/l and 10 µmol/l) before being stimulated with 5 ng/ml transforming growth factor ß1 (TGF-ß1). The viability and proliferation of cells were accessed by cell count kit-8 assay; Cell migration was examined by the wound closure assay; Alpha smooth muscle actin (α-SMA), connective tissue growth factor (CTGF) and type I collagen (COL I) transcription were detected by RT-qPCR; The expression and localization of α-SMA protein were examined by Western-blot analysis and Immunofluorescence staining; Western-blot analysis was also used to check the expression of CTGF, COL I peroxisome proliferator-activated receptor gamma (PPAR-γ), and phosphorylation of the signaling protein Smad2/3 RESULTS: Rosiglitazone is able to attenuate the up-regulation of α-SMA, CTGF, and COL I transcription, as well as affect protein expression, proliferation, and migration of cells; rosiglitazone also can increase PPAR-γ expression and attenuate Smad2/3 phosphorylation. CONCLUSIONS: Rosiglitazone can effectively attenuate activation of HTFs induced by TGF-ß1 without obvious toxicity. The possible mechanism might be that rosiglitazone interferes with TGF-ß/Smad signaling pathway.

Protective effects of human umbilical cord blood stem cell intravitreal transplantation against optic nerve injury in rats.

BACKGROUND: The majority of studies addressing traumatic optic neuropathy (TON) have focused on drugs, proteins, cytokines, and various surgical techniques. A recent study reported that transplantation of human umbilical cord blood stem cells (hUCBSCs) achieved therapeutic effects on TON, but the exact effects on optic nerve injury are still unknown, and the mechanisms underlying nerve protection remain poorly understood. METHODS: A total of 135 healthy Sprague-Dawley adult rats were randomly assigned to three groups: sham-surgery, model and transplantation, with 45 rats in each group. TON was induced in the model and transplantation groups via optic nerve crush injury. The crush injury was not performed in the sham-surgery group. Seven days after the injury, 10(6) hUCBSCs were injected into the rat vitreous cavity of transplantation group, and an equal volume of physiological saline was administered to the model and sham-surgery groups. Pathological observation of rat retina tissues was performed by hematoxylin-eosin (H&E) staining at days 3, 7, 14, 21 and 28 post-surgery. The number of retinal ganglion cells (RGCs) and mRNA expression levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) were assessed by the Fluorogold (FG) retrograde labeling and reverse transcriptase-polymerase chain reaction (RT-PCR) methods, respectively. RESULTS: The number of labeled RGCs and the expression of BDNF and GDNF mRNA obviously increased, and pathological injury was significantly ameliorated in the transplantation group compared to the model group (P < 0.05). CONCLUSIONS: Via intravitreal transplantation, the hUCBSCs resulted in a significant increase in the survival of the RGCs, and improved pathological changes in the rat retina, following TON. The protective mechanism is correlated with the continuous secretion of BDNF and GDNF in vivo of retina in optic nerve injury rats by the transplanted hUCBSCs.

Two cases of primary intraocular lymphoma: fine needle aspiration diagnosis and intravitreal methotrexate treatment.

We described clinical process of two cases of intraocular lymphoma in aspects of early diagnosis by fine needle aspiration (FNA) and biopsy and treatment by intravitreal methotrexate (MTX). Two patients were suspected to have primary intraocular lymphoma (PIOL) with geographic yellow-white infiltrates and vitreous opacity. FNA confirmed malignant intraocular lymphoma in one patient and failed in the other patient due to complication of vitreous hemorrhage. Subsequent vitreous biopsy confirmed malignant intraocular lymphoma in the other patient. Both patients were treated by intravitreal methotrexate. In case 1 the tumor had complete remission and follow-up of 12 months had not found any signs of recurrence. In case 2 the patient died of brain metastasis 22 months after the ocular biopsy. Our findings demonstrate that although cytological examination of vitrectomy specimens remains the gold standard in diagnosis of PIOL, examination of FNA and biopsy increases the reliability of early diagnosing or excluding a PIOL. Individualized intravitreal methotrexate can be used to effectively treat PIOL. More effective integrated program treating primary central nervous system lymphoma/PIOL is worthy of looking forward to.

Effect of Bak Foong Pills on the expression of ß-amyloid in rat retina with optic nerve transection.

AIM: To investigate the effect of Bak Foong Pills (BFP) on the expression of ß-amyloid (Aß) in rats retina with optic nerve transection, and its roles and possible mechanisms in protecting optic nerve damage. METHODS: Seventy-two healthy, Sprague-Dawley, adult rats were randomly assigned to three groups: negative control group (control group), optic nerve transection group (model group) and BFP treatment group (BFP group, 100µg/mL) followed by establishing optic nerve transection model. The expression of Aß was measured at 48 hours by Western-blotting. Moreover, the expressions of Bcl-2, Bax and Caspase-3 mRNA were evaluated at 48 hours by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: There were significant differences among the control, model and BFP groups in the expression of Aß (all P<0.01). Aß expression was significantly higher in the model and BFP groups than that in the control group (P<0.01), with a more significant reduction in the BFP group than that in the model group (P<0.01). Moreover, there were also significant differences among the three groups in the expressions of Bcl-2/Bax (Bcl-2: anti-apoptotic; Bax: proapoptotic) and Caspase-3 mRNA (proapoptotic) (all P<0.01). Bcl-2/Bax ratio was significantly lower and Caspase-3 mRNA expression was significantly higher in the model and BFP groups than those in the control group (P<0.01), with a significant growing of Bcl-2/Bax and reduction of Caspase-3 in the BFP group than those in the model group (P<0.01). CONCLUSION: BFP can down-regulate Aß expression in retina and may inhibit apoptosis and protect optic nerve by enhancing Bcl-2/Bax ratio and inhibiting Caspase-3 pathway.