High myopia (HM), characterized by significant ocular axial length elongation, affects hundreds of millions of people and is often inherited, particularly in cases that develop during childhood or adolescence. Although numerous myopia loci (MYP) have been identified, most causative genes remain undefined. Here, we analyzed two large HM pedigrees and refined the critical region through haplotype linkage analysis to a 3.9-Mb interval on 2q37.1, which was previously reported as MYP12 with an unknown pathogenic gene. Whole-genome sequencing identified the noncoding promoter variants c.-187G>T and c.-187G>C in PRSS56, encoding a trypsin-like serine protease, which exclusively co-segregated with all affected members in both pedigrees. Compared with matched controls, increased PRSS56 expression was observed in both patient-derived iPSCs carrying c.-187G>T and knock-in mice (c.-155G>T, corresponding to human c.-187G>T) that faithfully recapitulate myopia phenotypes. Noncoding PRSS56 variants promote self-expression via enhanced binding to the transcription factor EGR1, as confirmed by dual-luciferase assays. Notably, we demonstrated that higher PRSS56 levels directly increase ocular axial length in a dose- and activity-dependent manner in multiple transgenic mouse models. Guinea pig myopia models consistently exhibited high Prss56 expression, and short-wave light exposure reduced Prss56 mRNA levels and attenuated further axial elongation. Mechanistically, higher PRSS56 expression was associated with reduced abundance of myosin-4 in the sclera and with molecular signatures of scleral remodeling, which were in turn correlated with axial elongation. In conclusion, our findings provide strong genetic and functional evidence for the pathogenic role of noncoding PRSS56 variants in HM and highlight PRSS56 as a promising therapeutic target for juvenile HM.

Stem cell-derived secreted factors could protect neurons in neurodegenerative disease or after injury. The exact neuroprotective components in the secretome remain challenging to discover. Here we developed a cell-to-cell interaction model to identify a retinal ganglion cell (RGC)-protective factor derived from induced pluripotent stem cells (iPSCs). Primary RGCs were co-cultured with iPSCs or treated with iPSC-conditioned media in vitro. Cell viability were assayed using live-cell staining, and culture supernatant were analyzed via multiplexed antibody-based assays and ELISA. In vivo tests were carried out under mouse optic nerve crush model and RGC transplantation study in rats. Paired t-tests were used for data analysis between two groups. RGC viability was significantly enhanced when iPSCs were first stimulated with RGC-derived supernatant before iPSC-conditioned medium was collected and added into RGC culture. A significant increase of stem cell growth factor-beta (SCGF-β) concentration was detected in the latter conditioned medium. SCGF-β enhanced RGC survival in vitro and in vivo, and RGC-derived interleukin-12(p70) (IL-12[p70]) promotes secretion of iPSC-derived SCGF-β. Downstream of this IL-12(p70)-to-SCGF-β axis, ngn2 was significantly upregulated, and was found both necessary and sufficient for RGC survival. This study addresses a longstanding question of how neurons and stem cells interact to promote neuroprotection, and define a novel molecular interaction pathway whereby RGC’s secretion of IL-12(p70) enhances iPSCs’ secretion of SCGF-β, and SCGF-β protects RGCs via upregulating ngn2, suggesting that neurons may call on stem cells for their own protection.

Purpose: The purpose of this study was to characterize whether pulsed ultrasound (PUS) affects transscleral drug delivery. Methods: Fluorescein sodium (NaF, 376 Da) and fluorescein isothiocyanate-conjugated dextran 40 (FD-40, 40 kDa) were used as model drugs. Human sclera grafts were placed in modified Franz diffusion cells and were treated by PUS (1 megahertz [MHz], 0.71 W/cm2, duty cycle 30%, application time 5 minutes) once or repeatedly under various conditions to assess permeation enhancement and reservoir effect. The safety of PUS application was assessed on human sclera grafts ex vivo and rabbit eyes in vivo by histology and temperature measurements. Results: Single PUS application yielded a significant increase in FD-40 permeation (P < 0.05). Repeated PUS applications led to a further enhancement in FD-40 permeation and also significantly promoted NaF permeation (more than 8.51-fold, P < 0.05). The human scleral permeability was temporarily modified by PUS, as evidenced by the increased scleral permeability during PUS application and the unchanged permeability coefficients at steady state. The reservoir effect of human sclera was also enhanced by PUS application. Cavitation was detected under PUS. A minor increase in graft temperature rise (<1 degrees C) and no ocular damage was caused by PUS. Conclusions: PUS is an efficient and safe method to enhance model drugs to transport across human sclera by increasing the scleral permeability transiently and improving the reservoir effect. The enhancement was correlated with the molecule size and further promoted by the repeated PUS application. Translational Relevance: Our study provides proof of concept for using PUS to enhance drug delivery to the posterior eye segment.

This pilot study investigated the protective effect of transfecting brain-derived neurotrophic factor (BDNF) and B-cell lymphoma 2 (bcl-2) genes in retinal ganglion cells (RGCs) using in vivo electroporation in an adult rat optic nerve transection model. Sprague-Dawley rats were randomly divided into five groups: BDNF(+)/bcl-2(+), BDNF(+), bcl-2(+), empty plasmid (EP), and no surgery (NS). The plasmids were intravitreally injected and electroporated into the left eye. Seven days later, optic nerve transection was performed in all groups except the NS group. Protein expression was examined using Western blotting, RGC survival was quantified using 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate (DiI) retrograde labeling, and apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) at multiple time points (7, 14, and 28 d after transfection). A significantly higher number of DiI (+) RGCs and lower number of apoptotic cells were observed in the BDNF(+)/bcl-2(+), BDNF(+), and bcl-2(+) groups compared to those in the EP group at all time points. The number of DiI (+) RGCs in the three treatment groups was significantly lower than that in the NS group. However, there were no significant differences among the three treatment groups. The protective effects of gene transfection tended to be strongest in the BDNF(+)/bcl-2(+) group, followed by the BDNF(+) group and then the bcl-2(+) group. Thus, all gene transfection treatments had a protective effect against the loss of DiI(+) RGCs induced by optic nerve transection but did not result in full recovery. This study also confirmed the value of in vivo electroporation. The findings of this pilot study provide a working base for the development of gene therapy for blinding optic nerve disorders.

Retinal ganglion cells (RGCs) are susceptible to degenerative conditions such as glaucoma and traumatic optic neuropathies, which lead to vision loss. MicroRNA-21-5p has demonstrated potential neuroprotective effects, but its mechanisms in optic nerve injury remain underexplored. This study evaluates the neuroprotective role of microRNA-21-5p derived from induced pluripotent stem cells (iPSCs) in an optic nerve crush (ONC) model. In vitro qPCR demonstrated that the expression of microRNA-21-5p was increased in the co-culture medium of RGCs and iPSCs. Subsequently, in the in vivo experiments, we used a microRNA-21-5p agonist to assess its protective effects on RGCs. RNA sequencing was then performed in a mouse ONC model after treatment with a microRNA-21-5p agonist to explore the mechanisms underlying its neuroprotective effects on RGCs. As demonstrated in our previous experiments, the RGCs-iPSCs co-culture group led to a higher survival rate of RGCs, as indicated by live/dead cell staining, compared to the RGCs-only group. Quantitative PCR (qPCR) results revealed a significant increase in the expression of microRNA-21-5p in the medium of the RGCs-iPSCs co-culture group. Furthermore, the survival rate of mouse retinal RGCs treated with a microRNA-21-5p agonist was significantly greater than that of the control group. Lastly, RNA sequencing of the retina from microRNA-21-5p agonist-treated mice indicated that microRNA-21-5p plays a protective role in RGCs by downregulating the expression of several genes, including Irf1, Ccl4, Itk, Cxcr2, Dclre1c, Traf1, Traf2, Rbl1, Cxcl5, Cxcl3, Cxcl1, Cxcl9, Il2rg, Cd3e, Cd3d, Cxcl10, Ccl5, Ccl12, Tap1, and Cxcr4. MicroRNA-21-5p derived from iPSCs can enhance the survival rate of RGCs in the ONC model. This suggests that microRNA-21-5p may represent a novel and effective strategy for repairing RGC damage. Such a strategy could potentially be realized through the modulation of apoptosis, T-cell regulatory pathways, or TNF-α signaling.

Purpose: To investigate the efficacy and safety of pulsed ultrasound (PUS) in enhancing fluorescein sodium (NaF) transport to the rabbit eye through the transscleral and transconjunctival routes in vivo. Methods: PUS and NaF were applied onto the supratemporal sclera/conjunctiva of healthy rabbit eyes. PUS (1 MHz, 2.37 W/cm2, 30% duty cycle, 5-min application time) was performed 3 times with a 5-min interval. In the same process, NaF was administered to the eye without PUS in the control. NaF concentrations in the vitreous and retina-choroid were determined by fluorescence measurement. The safety of PUS application was assessed based on temperature and intraocular pressure measurements, clinical observations, electroretinography, histology, and Terminal Deoxynucleotidyl Transferase dUTP Nick End Labeling assay. Results: In comparison to the control, higher NaF concentrations were found in the retina-choroid following transscleral (2.45-fold) and transconjunctival (2.97-fold) PUS applications (P < 0.05). NaF concentrations in the vitreous were 3.15 and 5.86 times greater in transscleral and transconjunctival PUS applications, respectively, compared with those obtained without PUS application (P < 0.05), and NaF level in the vitreous after transconjunctival PUS application was 2.61 times that of transscleral PUS application (P < 0.05). Ocular findings were transient and mild conjunctival injection, with no other structural and functional changes in PUS-treated eyes. Conclusions: PUS treatment can improve transscleral and transconjunctival delivery of NaF efficiently and safely. Transscleral and transconjunctival PUS applications offer potential clinical benefit in increasing drug penetration to the posterior segments of the eye for the noninvasive treatment of ocular diseases.

Retinal prostheses could restore image-forming vision in conditions of photoreceptor degeneration. However, contrast sensitivity and visual acuity are often insufficient. Here we report the performance, in mice and monkeys with induced photoreceptor degeneration, of subretinally implanted gold-nanoparticle-coated titania nanowire arrays providing a spatial resolution of 77.5 μm and a temporal resolution of 3.92 Hz in ex vivo retinas (as determined by patch-clamp recording of retinal ganglion cells). In blind mice, the arrays allowed for the detection of drifting gratings and flashing objects at light-intensity thresholds of 15.70–18.09 μW mm–2, and offered visual acuities of 0.3–0.4 cycles per degree, as determined by recordings of visually evoked potentials and optomotor-response tests. In monkeys, the arrays were stable for 54 weeks, allowed for the detection of a 10-μW mm–2 beam of light (0.5° in beam angle) in visually guided saccade experiments, and induced plastic changes in the primary visual cortex, as indicated by long-term in vivo calcium imaging. Nanomaterials as artificial photoreceptors may ameliorate visual deficits in patients with photoreceptor degeneration. Gold-nanoparticle-coated titania nanowire arrays subretinally implanted in blind mice and monkeys offer advantages in visual acuity and contrast sensitivity towards the restoration of visual function.

Diabetic retinopathy (DR), the most common microvascular compilation of diabetes, is the leading cause of vision loss and blindness worldwide. Recent studies indicate that retinal neuron impairment occurs before any noticeable vascular changes in DR, and retinal ganglion cell (RGC) degeneration is one of the earliest signs. Axons of RGCs have little capacity to regenerate after injury, clinically leading the visual functional defects to become irreversible. In the past two decades, tremendous progress has been achieved to enable RGC axon regeneration in animal models of optic nerve injury, which holds promise for neural repair and visual restoration in DR. This review summarizes these advances and discusses the potential and challenges for developing optic nerve regeneration strategies treating DR.

The aim of this study was to investigate the effects of 7,8-dihydroxyflavone (7,8-DHF) in protecting retinal ganglion cells (RGCs) and promoting axonal regeneration, and to explore its potential molecular mechanisms. We used three-dimensional retinal culture system and optic nerve crush (ONC) rat models in this study. The pro-axonal regenerative effect of 7,8-DHF was determined with light microscopy observation and immunofluorescence staining of Thy1.1 and GAP43. The RGC protective function of 7,8-DHF was detected by RBPMS immunofluorescent staining and TUNEL staining. The inhibition effect of 7,8-DHF on astrocyte activation was measured using GFAP immunofluorescence and Western blotting. The protein levels of p-TrkB, p-AKT and p-ERK was examined by Western blotting and immunohistochemistry. Our results revealed that 7,8-DHF significantly promoted the average density and length of regenerated neurites and suppressed the apoptosis of GCL cells in three-dimensional culture system and significantly increased the number of RBPMS-positive cells and inhibited the GFAP expression and apoptosis of GCL cells in ONC rats. Our results also revealed that 7,8-DHF activates TrkB, AKT and ERK proteins in vivo, however, these activations can be inhibited byANA-12. In conclusion, 7,8-DHF protects RGCs and promotes axonal regeneration through the TrkB signaling pathway followed by AKT and ERK activation.

1 近视的成因 我国是近视大国,全国近视患者超过6亿,近视率为世界第一.疫情以来,随着网课等线上教育增加,近视问题更加成为社会关注的热点.

Purpose: This study aimed to investigate the simultaneous neuroprotective and proangiogenic effects of 7,8-dihydroxyflavone (7,8-DHF) and explore the potential underlying molecular mechanisms. Methods: A coculture system of rat retinal explants and human umbilical vein endothelial cells (HUVECs) was established to determine the optimal concentration of 7,8-DHF, promoting neurite regeneration and HUVEC proliferation. Subsequently, the neuroprotective effect, proangiogenesis properties, and action mechanism of 7,8-DHF at an optimal concentration were investigated. Results: The cell proliferation, survival, migration, tube formation and p-tropomyosin-related kinase receptor B (TrkB)/TrkB levels in HUVECs were significantly promoted by 5 μM 7,8-DHF. The ganglion cell layer neuron survival, neurite regeneration, and p-TrkB/TrkB levels in retinal explants were also significantly promoted by 5 μM 7,8-DHF. All of these pharmacological actions of 7,8-DHF were blocked by N-[2-[(2-oxoazepan-3-yl)carbamoyl]phenyl]-1-benzothiophene-2-carboxamide. Conclusions: 7,8-DHF yields neuroprotection of retinal explants and proangiogenesis of HUVECs through the TrkB signaling pathway in vitro.

在医院"双一流"建设过程中,一支能支撑起一流学科创新发展的人才队伍是关键.高校附属专科医院不仅拥有较高的专科学术地位、初具规模的研究人才、所属高校入选"双一流学科建设大学"等优势和机会,还面临部分亚专科人才梯队不完备、多学科支撑薄弱、公立综合医院快速发展和民营专科医院涌现等劣势和威胁.必须要牢牢抓住人才队伍建设,通过引育创新型人才、完善临床研究专职人员队伍建设、注重医工学科交叉融合、制订有效的人才激励机制、注重医院文化建设等措施,才能推动医院向研究型专科医院转型.

Background: Three-dimensional culture system of retinal explant is commonly used to study retinal ganglion cell (RGC) axon regeneration in vitro. The retinal explants fabricated by traditional procedure in culture system, however, are usually too small (merely 0.5 x 0.5 mm) to be easily detected or treated by current experimental techniques. Also, the constituents of culture medium have not been fully elucidated. New method: A fabrication procedure was developed to enlarge the retinal explants and explore the reasonable concentration of fetal bovine serum (FBS) for evaluating axonal regeneration. Results: There were no significant differences in the density or length of regenerative neurites in the retinal explants fabricated by traditional and modified procedures. Increased FBS concentrations promoted neurite regeneration, decreased RGCs apoptosis, and activated tyrosine kinase B (TrkB) receptors, all reaching a plateau at 1 % FBS. Comparison with existing methods: Compared with traditional procedure, the modified fabrication procedure facilitates application of experimental techniques to retinal explants, increases the efficiency of obtaining observation area of regenerating neurites, and reduces the wastage of retinal tissues. The recommended FBS concentration determined in this study is shown to be more suitable for studying neuronal regeneration. Conclusion: The retinal explants made by the modified fabrication procedure are successfully applied to the three-dimensional culture system, and presented several advantages over the traditional one. Furthermore, a preliminary experiment must be performed to determine the suitable concentration of FBS in each study to ensure accuracy and stability of the results obtained from the three-dimension retinal culture system.

Abstract Background: This study aimed to investigate the anti-angiogenesis effect of 7,8-dihydroxyflavone (7,8-DHF) and its potential molecular mechanism. Methods: The rhesus macaque choroid-retinal endothelial (RF/6A) cells were treated with different concentrations (from 0 to 100 μM) of 7,8-DHF and/or 40 ng/ml VEGF. The morphology, proliferation, migration, capillary-like tube formation，and apoptosis of RF/6A cells were evaluated by Giemsa staining, CCK-8 assay, transwell migration assay, matrigel tube formation assay, and flow cytometry/hoechst33342 staining, respectively. The protein content of VEFGR2 and p-VEGFR2 was assessed by western blotting. Results: 7,8-DHF significantly inhibited the proliferation, migration, and tube formation of RF/6A cells and promoted their apoptosis in vitro. The expression of VEGFR2 in RF/6A cells was constant whether or not to administer 7,8-DHF. However, the phosphorylation of VEGFR2 significantly decreased after the administration of 7,8-DHF. Conclusions: 7,8-DHF could inhibit RF/6A angiogenesis in vitro. The inhibitory mechanism of 7,8-DHF in angiogenesis was attributed to the suppression of VEGFR2 phosphorylation and thus blocking of VEGF/VEGFR2 signal pathway.

Ocular drug delivery, specifically protein drug delivery to the posterior segment of the eye, remains a challenge. The purpose of this study was to prepare a new double-controlled drug release system (with insulin as the drug) for ocular delivery via subconjunctival injection and to investigate its ocular biocompatibility and safety. The double-controlled release system, insulin-loaded nanoparticles/PLGA-PEG-PLGA hydrogel (ICNPH) was prepared by adding insulin-loaded chitosan nanoparticles (ICN) to PLGA-PEG-PLGA hydrogel. The characteristics of the ICN were determined by dynamic light scattering and scanning electron microscopy. HPLC was used to analyze the loading content and insulin release profile of the ICNPH. The ICN were found to be globular particles with a mean diameter of 137.5 nm and 12% loading content. The sustained release of insulin from the ICNPH lasted for more than 60 days. Electroretinograms, retinal ultrastructure and microstructure, retinal cell apoptosis and glial fibrillary acidic protein expression were examined to assess retinal injury caused by the ICNPH after subconjunctival injection. The results showed no obvious damage to retinal function, structure and neurons. Therefore, the ICNPH is biocompatible and safe via subconjunctival injection, and may be a candidate for ocular drug delivery.

Objective To compare the effect of herb monomers (puerarin,tetramethylpyrazine,bilobalide-B and saffron-I) on promoting regeneration of axons of retinal ganglion cell (ARGC) in rat.Methods The retina of SD rats aged 1-3d were cut into pieces of 0.5mm × 0.5mm,and cultured in three-dimensional culture system.The tissues of experimental group were cultured in culture medium with different concentration of puerarin,tetramethylpyrazine,bilobalide-B and saffron-I (0.125g/L,0.25 g/L,0.5 g/L,1.0 g/L),while control group only cultured with normal medium.The growth of RGCs axons were investigated by fluorescence inverted microscopy and immunohistochemical staining.The number and length of outgrowing RGC axons were calculated in the 3rd,6th and 9th day.The effect of different herb monomers and concentrations on regeneration of ARGC were compared.The regeneration axons with Thy-1.1 and GAP-43 by immunohistochemical staining in the 6th day were tested.Results The number of regrowing axons of all experimental groups were larger and the length was longer than which in the control group,among which the effect of bilobalide-B group was the most obvious (P ＜ 0.05).Thy-1.1 and GAP-43 double positive fibers shown to be regenerated axons.Conclusion Puerarin,tetramethylpyrazine,bilobalide-B and saffron-I could improve the regeneration and elongation of cultured RGCs axons,and bilobalide-B could be the most effective one.

Purpose:To investigate whether reduced Sox9 function exerts neuroprotection in light-induced retinal damage in rats and to explore the potential mechanism behind it. Methods:Retinal light damage was used as a model for retinal degeneration. Two weeks before light damage in adult Sprague Dawley (SD) rats, the Sox9-shRNA lentiviral vector was intravitreally injected. On days 3, 7, and 14, retinal function was assessed using electroretinography (ERG), and the thickness of the outer nuclear layer (ONL) was measured in hematoxylin and eosin (HE) stained sections. The protein levels of glial fibrillary acidic protein (GFAP), vimentin, nestin, and chondroitin sulfate proteoglycans (Cspgs), which are related to gliosis and extracellular matrix (ECM) remodeling, were observed using western blot analysis. The expression of GFAP was further evaluated by immunohistochemistry. Results:On days 3, 7, and 14 after light damage, the thickness of the ONL and the amplitudes of the ERG waves were significantly better preserved in the Sox9-shRNA group when compared with the control group. The protein levels of GFAP, vimentin, nestin, and Cspgs were significantly downregulated in the Sox9-shRNA group. Furthermore, the staining intensity and the spatial distribution of GFAP in the retinas were also obviously attenuated at every studied time point. Conclusions:Intravitreal injection of the Sox9-shRNA lentiviral vector preserved rat retinal morphology and function after light damage and downregulated GFAP, vimentin, nestin, and Cspgs, which are related to Müller cell gliosis and ECM remodeling. The results indicate that Sox9 might be a potential therapeutic target for retinal degenerative diseases.

BACKGROUND:To pursuit effective sustained release systems for insulin to treat diabetic retinopathy (DR), a novel insulin delivering system was developed via loading onto chitosan nanoparticles/poly(lactic-co-glycolic acid)-poly(ethylene glycol)-poly(lactic-co-glycolic acid) hydrogel (ICNPH).METHODS AND MATERIALS:Examinations including electroretinography, HE staining, transmission electron microscopy, terminal deoxynucleotidyl transferased UTP nick-end labeling, immunofluorescence, Western blot, and real-time polymerase chain reaction were performed to evaluate the neuroprotective efficacy of ICNPH on DR by a single subconjunctival injection.RESULTS:Compared with the insulin, blank, and sham treatment groups, subconjunctival injection of ICNPH significantly reduced the decrease of scotopic B-wave amplitude, alleviated retinal micro- and ultrastructural changes, and reduced retinal cell apoptosis caused in DR rats. Meanwhile, a significant reduction of vascular endothelial growth factor and glial fibrillary acidic protein expression as well as a remarkable increase in Occludin expression was also found in retinas in ICNPH group compared with the sham treatment group.CONCLUSION:The results indicate that ICNPH has sufficient neuroprotective effect on retinas through subconjunctival injection in DR rats and facilitates controlled insulin delivery. It might be one of the therapeutic strategies for DR in the near future.

Objective To investigate whether the protective effects of leonurine (SCM-198) against endotoxin induced uveitis (EIU) of SD rats caused by lipopolysaccharide (LPS) was existing,and discuss the underlying mechanisms.Methods Thirty-six normal healthy male SD rats were divided into 3 groups randomly with the same baseline bodyweight and feeding conditions.All rats received intragastric administration every day.The experimental group was devided into 4 subgroups,rats in these subgroups received SCM-198 intragastric administration by as the dose of 10,20,40 and 80 mg/kg bodyweight per day,rats in the negative control group received intragastric administration of normal saline 10 mL/kg per day,rats in the positive control group received intragastric administration ofdexamethasone (DEX) 0.5 mg/kg bodyweight per day.All rats received a 21-day-intragastric administration.The body weight of all rats was monitored every 7 days.The electroretinogram (ERG) examination was taken in the 18th day.All rats received a 100 mg S.typhi LPS intraperitoneal injection after the 21st intragastric administration.Twenty-four hours later,following anaesthesia,all rats received another ERG examination,and inflammation was scoring under microscope by 2 experienced ophthalmologists,after that the aqueous humor of all rats was collected from the left eye.The aqueous humor was kept in-80 ℃ immediately.Then the rats were sacrificed and the right eyes were immediately enucleated to finish the HE staining and immunohistochemistry (IHC) staining examination of tumor necrosis factor-α (TNF-α) and intercellular cell adhesion molecule-1 (ICAM-1).The total amount of protein in aqueous humor was detected by BCA test.Western blot was used to examine the expression of TNF-α,interleukin-1β (IL-1β),IL-6 and ICAM-1.All data was analyzed by SPSS 19.0,and differences were considered significant at P＜0.05.Results The body weight of the rats in positive control group was significantly lower (P＜0.05) than the experimental group and the negative control group after the 21-day-intragastric administration.The inflammatory score of experimental group was lower than that of the negative control group,but higher than the score of positive control group.The HE staining sections showed the similar results.The a wave of ERG in 0.01 cd of rats received 20 mg/kg SCM-198 daily intragastric administration after LPS injection was significantly lower than that before the LPS injection (P＜0.05),also lower than other groups after LPS injection.The expression of TNF-α,IL-6 and IL-1β in the aqueous humor of the rats in the subgroup of SCM-198 10 mg/kg daily intragastric administration was lower than other groups.Conclusions Intragastric administration of SCM-198 has protective effect against endotoxin induced uveitis in SD rats without obvious adverse reaction,which could alleviate the imflammatory reaction and the damage to the uvea construction.NF-κB plays an important role in the reaction.Thus,SCM-198 is a candidate potent compound with potential therapeutic applications in inflammation associated eye diseases.While the best mode and dose of administration should be further investigated.

Anisometropia is one of the most common refractive error types of children.Anisometropia always impairs the visual acuity,as well as the binocular visual function of children.Anisometropia is also the main cause of amblyopia in elder children and adults.This article reviews the clinical research progress in epidemiology,visual function,diagnosis and treatment of children's anisometropia.