The role of Islet-1 in cell specification,differentiation,and maintenance of phenotypes in the vertebrate neural retina

Many blinding diseases,such as retinitis pigmentosa,age-related macular degeneration,and glaucoma involve the permanent loss of retinal neurons,especially photoreceptors or the centrally projecting retinal ganglion cells.Stem cells have been proposed as a potential source of cells for neuronal transplantation.

New antioxidant SkQ1 is an effective protector of rat neural retina under conditions of long-term organotypic cultivation

During life human eye is constantly exposed to sunlight and artificial light, the sources of reactive oxygen species (ROS)—the main cause of age-related eye pathology. A novel mitochondria-targeted antioxidant SkQ1 has recently been invented to reduce mitochondrial ROS by cleaning the mitochondria matrix, “the dirtiest place in the cell” in respect of ROS production and accumulation. Earlier we studied SkQ1 effects upon retinal pigment epithelium and choroid in the rat eye posterior cups exposed to long-term 3D organotypic culturing. It was found that under in vitro conditions 20 nM SkQ1 effectively reduced cell death in retinal pigment epithelium and choroid and protected the tissues from disintegration and cell withdrawal. In the present study we used same ex vivo conditions to examine the effect of SkQ1 upon the rat neural retina kept in the content of the posterior eye cup. Eye cups were isolated and cultured in vitro during 7, 14, and 30 days under rotation in the presence and absence of 20 nM SkQ1 in the culture medium. Serial sections of cultivated eye cups were subjected to histology, computer morphometry and immunohistochemistry. Obtained results show that SkQ1 operates as a strong protective agent, preventing neuronal cell death and other degenerative processes in the neural retina. Cell rescue by SkQ1 was more vivid in the central part of the retina than at the periphery. That, in turn, suggests SkQ1 effectiveness in treatment of some age-related eye diseases when central part of the retina, including macula, is most susceptible to degeneration.

Endogenous retinal neural stem cell reprogramming for neuronal regeneration

In humans, optic nerve injuries and associated neurodegenerative diseases are often followed by perma- nent vision loss. Consequently, an important challenge is to develop safe and effective methods to replace retinal neurons and thereby restore neuronal functions and vision. Identifying cellular and molecular mechanisms allowing to replace damaged neurons is a major goal for basic and translational research in regenerative medicine. Contrary to mammals, the zebrafish has the capacity to fully regenerate entire parts of the nervous system, including retina. This regenerative process depends on endogenous retinal neural stem cells, the Miiller glial cells. Following injury, zebrafish Miiller cells go back into cell cycle to proliferate and generate new neurons, while mammalian Mtiller cells undergo reactive gliosis. Recently, transcription factors and microRNAs have been identified to control the formation of new neurons derived from ze- brafish and mammalian Mtiller cells, indicating that cellular reprogramming can be an efficient strategy to regenerate human retinal neurons. Here we discuss recent insights into the use of endogenous neural stem cell reprogramming for neuronal regeneration, differences between zebrafish and mammalian Mtiller cells, and the need to pursue the identification and characterization of new molecular factors with an instructive and potent function in order to develop theurapeutic strategies for eye diseases.

Spatiotemporal alterations of presynaptic elements in the retina after high intraocular pressure

A rat model of acute high intraocular pressure was established by injecting saline into the anterior chamber of the left eye. Synaptophysin expression was increased in the inner plexiform layer at 2 hours following injury, and was widely distributed in the outer plexiform layer at 3-7 days, and then decreased to the normal level at 14 days. This suggests that expression of this presynaptic functional protein experienced spatiotemporal alterations after elevation of intraocular pressure. There was no significant change in the fluorescence intensity and distribution pattern for synapse-associated protein 102 following elevated intraocular pressure. Synapse-associated protein 102 immunoreactivity was confined to the outer plexiform layer, while synaptophysin immunoreactivity spread into the outer plexiform layer and the outer nuclear layer at 3 and 7 days following injury. These alterations in presynaptic elements were not accompanied by changes in postsynaptic components.

Viability of primary cultured retinal neurons in a hyperglycemic condition

The retina of Wistar rats within 1-3 days of birth were dissociated into a retinal ceil suspension using 0.05% trypsin digestion. The cell suspension was incubated in Dulbecco＇s modified Eagle＇s medium for 24 hours, followed by neurobasal medium for 5-7 days. Nissl staining showed that 79.86% of primary cultured retinal cells were positive and immunocytochemical staining showed that the purity of anti-neurofilament heavy chain antibody-positive cells was 71.53%, indicating that the primary culture system of rat retinal neurons was a reliable and stable cell system with neurons as the predominant cell type. The primary cultured retinal neurons were further treated with 0, 5.5, 15, 25, and 35 mM glucose for 24, 48, and 72 hours. The thiazolyl blue tetrazolium bromide test and flow cytometry showed that with increasing glucose concentration and treatment duration, the viability of retinal neurons was reduced, and apoptosis increased. In particular, 35 mM glucose exhibited the most significant effect at 72 hours. Thus, rat retinal neurons treated with 35 mM glucose for 72 hours can be used to simulate a neuronal model of diabetic retinopathy.

The Schlager mouse as a model of altered retinal phenotype

Hypertension is a risk factor for a large number of vision-threatening eye disorders.In this study,we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse(Schlager mouse)and compared it to its control counterpart,the normotensive BPN/3J strain.The BPH/2J mouse is a selectively inbred mouse strain that develops chronic hypertension due to elevated sympathetic nervous system activity.When compared to the BPN/3J strain,the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age,which was indicative of a severe vision-threatening disease potentially caused by hypertension.To elucidate whether the retinal neural phenotype in the BPH/2J strain was attributed to increased BP,we investigated the neural retina of both BPN/3J and BPH/2J mice at 4 weeks of age.Our preliminary results showed for the first time that the BPH/2J strain develops severe retinal neural damage at a young age.Our findings suggest that the retinal phenotype in the BPH/2J mouse is possibly due to elevated blood pressure and may be contributed by an early onset spontaneous mutation which is yet to be identified or a congenital defect occurring in this strain.Further characterization of the BPH/2J mouse strain is likely to i)elucidate gene defects underlying retinal disease;ii)understand mechanisms leading to neural retinal disease and iii)permit testing of molecules for translational research to interfere with the progression of retinal disease.The animal experiments were performed with the approval of the Royal Perth Hospital Animal Ethics Committee(R535/17-18)on June 1,2017.

Effect of ciliary neurotrophic factor on bcl-2 and c-jun gene and protein expression in cultured retinal nerve cells

BACKGROUND：In various retinal neurodegenerative animal models,ciliary neurotrophic factor （CNTF） exhibits prominent neuroprotective effects on retinal nerve cells.Bcl-2 is an anti-apoptotic protein.c-Jun is upregulated and phosphorylated in the activated c-Jun N-terminal kinase pathway,which subsequently mediates apoptosis.However,the effect of CNTF on Bcl-2 and c-Jun expression in retinal nerve cells remains unclear.OBJECTIVE：To determine the dynamic changes in retinal nerve cell apoptosis,as well as bcl-2 and c-jun gene and protein expression,following a single dose of CNTF in a short period of time.DESIGN,TIME AND SETTING：A single-blind,randomized,controlled,in vitro experiment was performed at the Central Laboratory of Beijing Tongren Hospital from May 2008 to April 2009.MATERIALS：Neonatal bovine retinal nerve cells （Chinese Holstein）,recombinant human CNTF （PeproTech,Rocky Hill,NJ,USA）,rabbit polyclonal anti-Bcl-2 and c-Jun antibodies （Abeam,Cambridge,UK）,fluorescein isothiocyanate-conjugated annexin V/propidium iodide kit （BioVision,Mountain View,CA,USA）,real time polymerase chain reaction instrument （ABI,Foster City,CA,USA）,and flow cytometer （BD FACSCalibur,Franklin Lakes,NJ,USA）.METHODS：Neonatal bovine retinal cells from passage 2 were cultured for 3 days and incubated with,or without,50 ng/mL CNTF （control）.MAIN OUTCOME MEASURES：Cell apoptosis was detected via Annexin V-FITC/PI double-staining and flow cytometry.bcl-2 and c-jun mRNA and protein expression were detected by quantitative real time polymerase chain reaction and western blot analysis.RESULTS：The proportion of late-stage apoptotic cells was significantly decreased at 2,4,and 6 days after CNTF treatment compared with the control group （P 〈 0.01）.CNTF did not alter bcl-2 mRNA expression at the three time points,but significantly increased Bcl-2 protein expression at 2 and 4 days （P 〈 0.01）.c-jun mRNA expression was significantly decreased 4 days after CNTF treatment （P〈 0.01）.In addition,c-Jun protein expression was slightly increased at 4 days （P〈 0.01）,but decreased at 6 days,compared with the control group （P〈 0.05）.CONCLUSION：A single dose of CNTF （50 ng/mL） upregulated Bcl-2 protein and downregulated c-jun mRNA expression,followed by a parallel,but lagged,change in c-Jun protein production in cultured neonatal bovine retinal nerve cells.These results suggested that CNTF reduces retinal nerve cell apoptosis by modifying Bcl-2 and c-Jun expression.

Beta-amyloid precursor protein cleavage enzyme-1 expression in adult rat retinal neurons in the early period after lead exposure

Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein （Aβ）,and exhibit upregulation of β-site amyloid precursor protein expression in old age.However,further evidence is required to elucidate the precise relationship and molecular mechanisms underlying the effects of early lead exposure on excessive Aβ production in adult mammals.The present study investigated the effects of lead exposure on expression of β-amyloid precursor protein cleavage enzyme-1 （BACE-1） in the rat retina and the production of Aβ in early development,using the retina as a window for studying Alzheimer＇s disease.Adult rats were intraocularly injected with different doses of lead acetate （10μmol/L,100μmol/L,1 mmol/L,10 mmol/L and 100 mmol/L）.The results revealed that retinal lead concentration,BACE-1 and its cleavage products β-C-terminal fragment and retina Aβ1-40 were all significantly increased in almost all of the lead exposure groups 48 hours later in a dose-dependent manner.The only exception was the 10μmol/L group.The distribution of BACE-1 in the retina did not exhibit obvious changes,and no distinctive increase in the activation of retinal microglia was apparent.Similarly,retinal synaptophysin expression did not exhibit any clear changes.These data suggest that lead exposure can result in the upregulation of retinal neuron BACE-1 expression in the early period of development and further increase the overproduction of Aβ1-40 in the retina.Our results provided novel insight into the molecular mechanisms underlying environmentally-induced Alzheimer＇s disease.

Pathological changes in the retina and growth associated protein-43 expression following treatment of intracanalicular optic nerve injury via optic canal decompression,dexamethasone or their combination

BACKGROUND： The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones, but both treatments have disadvantages. OBJECTIVE： To observe the pathological changes in the retina and growth associated protein-43 （GAP-43） expression, to compare the treatment of optic canal decompression, hormones, and their combination with the intracanalicular optic nerve injury.DESIGN, TIME AND SETTING： A randomized, controlled animal study was performed at the Department of Anatomy, Weifang Medical University, China, from September 2007 to November 2008.MATERIALS： Dexamethasone （Shandong Huaxin Pharmaceutical, China） and rabbit anti-GAP-43 polyclonal antibody （Boster, China） were used.METHODS： All 36 healthy adult rabbits were randomly assigned to control group （n = 4）, simple injury group （n = 20）, and treatment group （n = 12）. Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method. The control group was left intact. The treatment group （four rabbits in each subgroup） was treated by optic nerve decompression, dexamethasone treatment （1 mg/kg daily via two intravenous infusions, 1/5 total dose reduction every 3 days, for 14 days）, and simultaneously giving surgery and hormone treatment.MAIN OUTCOME MEASURES： Pathological changes in the retina were determined using hematoxylin-eosin staining. GAP-43 expression was detected using immunohistochemistry in the retina.RESULTS： Retina injury induced obvious pathological changes in the retina. With prolonged time after optic nerve injury, the number of retinal ganglion cells was gradually decreased, and reached the minimum on day 14 （P〈0.01）. All three treatments increased the number of retinal ganglion cells （P〈0.01）, but surgery ＋ hormone treatment was most effective. No GAP-43 cells were present in the normal retinal, but they appeared 3 days after injury, peaked 7 days after injury, and then began to decline.CONCLUSION： Intracanalicular optic nerve injury induced obvious pathological changes in the retina, including increased GAP-43 expression. Optic canal decompression and hormones improved nerve repair after injury, and their combination produced better outcomes.

TrkB and p-trkB expression in brain-derived neurotrophic factor-pretreated rat retina following acute high intraocular pressure

BACKGROUND： Exogenous brain-derived neurotrophic factor （BDNF） promotes retinal ganglion cell survival. However, the protective mechanisms remain unclear. OBJECTIVE： To investigate changes in retinal tyrosine kinase receptor B （trkB） expression and effects of exogenous BDNF on trkB activation in a rat model of acute high intraocular pressure （HtOP）. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Anatomy and Neurobiology, Xiangya Medical School, Central South University from January 2004 to August 2006. MATERIALS： Rabbit anti-BDNF and anti-trkB.FL（full-length） polyclonal antibodies were purchased from Santa Cruz Biotechnology, USA; rabbit anti-p-trkB polyclonal antibodies were purchased from Cellsignal, USA. METHODS： A total of 48 healthy, adult, Sprague Dawiey rats were randomly assigned to acute HIOP （without BDNF pre-treatment） and BDNF pre-treated groups, with 24 animals in each group. In the BDNF pre-treated group, the left eyes were intravitreally injected with 3 pg/kg BDNF 2 days prior to HIOP. Rats in the acute HIOP group were not pre-treated with BDNE HIOP models were established by increased intraocular pressure in the left eyes until the b-wave of flash electroretinogragh disappeared and pressure was maintained for 60 minutes. The right eyes of all rats were not treated and served as the normal controls. MAIN OUTCOME MEASURES： Retinal structure and cell numbers in the ganglion cell layer （GCL） were detected by Nissl staining; expression of trkB and phosphorylated trkB in the rat retina were determined by immunohistochemistry. RESULTS： A greater number of GCL neurons were observed in the pre-treated group compared to the acute HIOP group （P 〈 0.05）. TrkB expression was significantly increased following HIOP at days 1 and 3 （P 〈 0.05）, but expression varied between retinal areas. Although trkB expression decreased at 7 days, phosphorylated trkB dramatically decreased with increasing time （P 〈 0.05）. TrkB expression in BDNF pre-treated rats was similar to the acute HIOP group at early injury time points. Nevertheless, trkB expression was significantly decreased compared to the acute HIOP group at 7 days （P 〈 0.05）, and phosphorylated trkB expression was significantly greater compared to the acute HIOP group at each time point （P〈 0.05）. CONCLUSION： TrkB expression displayed temporal and spatial changes in the rat retina following acute HIOP, and trkB up-regulation suggested that more BDNF was required for treating the injured retina. Exogenous BDNF partially ameliorated decreased expression of phosphorylated trkB and provided protection to the injured retina, to a certain degree, following HIOP.

基于卷积神经网络的农作物智能图像识别分类研究

首先,介绍了卷积神经网络结构、各个模块的工作原理和Retina-Net目标检测算法;然后,采用颜色直方图特征提取方法,实现了卷积神经网络的农作物智能图像识别分类算法。实验结果表明:该算法可以准确地对番茄枝上的番茄进行识别测试,且准确率较高,有效性和准确性强,能够满足实时果实识别的应用需要。

视网膜功能启发的边缘检测层级模型

基于视网膜对视觉信息的处理方式,提出一种视网膜功能启发的边缘检测层级模型.针对视网膜神经元在周期性光刺激下产生适应的特性,构建具有自适应阈值的Izhikevich神经元模型;模拟光感受器中视锥细胞、视杆细胞对亮度的感知能力,构建亮度感知编码层;引入双极细胞对给光-撤光刺激的分离能力,并结合神经节细胞对运动方向敏感的特性,构建双通路边缘提取层;另外根据神经节细胞神经元在多特征调控下延迟激活的现象,构建具有脉冲延时特性的纹理抑制层;最后将双通路边缘提取的结果与延时抑制量相融合,得到最终边缘检测结果.以150张来自实验室采集和AGAR数据集中的菌落图像为实验对象对所提方法进行验证,检测结果的重建图像相似度、边缘置信度、边缘连续性和综合指标分别达到0.9629、0.3111、0.9159和0.7870,表明所提方法能更有效地进行边缘定位、抑制冗余纹理、保持主体边缘完整性.本文面向边缘检测任务,构建了模拟视网膜对视觉信息处理方式的边缘检测模型,也为后续构建由视觉机制启发的图像计算模型提供了新思路.

一种用于黄斑病变分类的改进卷积神经网络模型

基于卷积神经网络的视网膜黄斑病变自动识别技术可辅助眼科医生诊断黄斑病变。为解决黄斑病变区域小和特征不明显导致黄斑病变类型不易识别的问题,提出了一种用于黄斑病变分类的改进卷积神经网络模型。首先,加入多尺度特征融合模块,将带有不同感受野的特征图进行拼接,从而提取更加丰富的黄斑病变特征;其次,增加注意力机制,有效抑制冗余特征的同时增加对病变区域的关注;最后,引入有效样本加权损失函数,充分学习少样本类别的病变特征,从而解决数据样本不平衡问题。实验证明,在UCSD视网膜黄斑病变数据集上,提出的模型进一步提高了黄斑病变的分类效果,分类准确率达到了97.60%,能够更加有效地辅助眼科医生诊断黄斑病变,提高诊疗效率。

质谱法分析2型糖尿病大鼠神经视网膜差异表达蛋白

采用二维电泳(2DE)分离了正常SD大鼠和2型糖尿病模型大鼠神经视网膜组织总蛋白,并用ImageMaster5.0软件分析比较了正常组和糖尿病组2DE图像,正常组检测到3122±37(n=3)个蛋白质点;糖尿病组检测到2702±21(n=3)个蛋白质点.约150个蛋白质点的表达水平在两组之间存在明显差异(P<0.05).在糖尿病组中表达上调的点68个,下调的点82个.选择20个差异表达蛋白质点进行肽质量指纹谱(PMF)或串联质谱鉴定,其中7个蛋白已有报道与糖尿病视网膜病变(DR)相关,10个蛋白尚未见有报道.

脊髓神经干细胞对小鼠视网膜移植的研究

目的 研究原代培养的脊髓神经干细胞在小鼠视网膜的整合和分化情况。 方法 利用细胞培养和体内移植技术 ,将原代脊髓神经干细胞 (NSC)移植到不同年龄小鼠的视网膜 ,并对移植后细胞的整合及分化情况进行了免疫组织化学分析。 结果 1 移植的NSC对组织的整合能力随宿主年龄的增加而降低 ;2 移植的NSC在宿主视网膜内可以分化为星形胶质细胞、少突胶质细胞和神经元。 结论 脊髓原代NSC移植到小鼠视网膜后的整合和分化均受内外因素的调控 。

人视网膜中神经干细胞样细胞的分离和体外培养

目的 分离培养发育基本成熟的人视网膜中神经干细胞样细胞。方法 取 0～ 3岁猝死婴幼儿视网膜细胞 ,在干细胞选择性培养基中培养 ,观察原代和传代细胞的形态和增殖情况 ,并对其诱导分化。通过免疫细胞化学方法检测Nestin、MAP 2和GFAP的表达。结果 原代细胞可形成悬浮生长的致密球状细胞团 ,传代后能形成新的细胞球。部分细胞球表达Nestin ,传代后阳性率增加。分化后细胞形态多样 ,每一团细胞相对一致 ,部分细胞表达MAP 2或GFAP。结论 0～ 3岁人视网膜中存在一种表现出神经干细胞特性的细胞。

神经干细胞玻璃体内移植后的分化及对视网膜节细胞的影响

目的:观察视神经(ON)微挤压断后玻璃体内移植神经干细胞(NSCs)的分化情况及其对视网膜节细胞(RGCs)轴突再生的促进作用。方法:在成年大鼠球后1mm处微挤压断ON,在玻璃体内注入Hoechst33342标记的NSCs2×104个,实验动物分对照组(MC组、MC+PBS组)、实验组(MC+NSCs组),各组动物分别存活3、4、5周。用粒蓝逆行标记再生的RGCs,在荧光镜下观察视网膜平铺片再生RGCs的数量变化。另取实验组5只动物存活4周后取眼球切片观察NSCs分化情况。结果:存活3、4、5周,再生的RGCs数目实验组与对照组有显著差异(P<0.01)。4周后移植的NSCs表达NF、CNP、GFAP;未见NSCs迁移至视网膜内。结论:玻璃体内注入NSCs可显著促进ON微挤压断后RGCs轴突的再生,并在玻璃体内分化为神经元、星形胶质细胞和少突胶质样细胞。

大鼠胚胎视网膜中神经干细胞的体外培养与鉴定

目的培养和鉴定大鼠胚胎视网膜中的神经干细胞。方法取孕龄16～19dSD大鼠胚胎鼠的视网膜组织,在干细胞选择性培养基中培养,用免疫组织化学法来检测Nestin和Chx-10的表达。结果SD大鼠胚胎鼠视网膜中的神经干细胞在体外悬浮生长,形成致密的球形细胞团,传代后能够生成新的细胞团,原代和传代细胞Nestin和Chx-10蛋白均表达阳性。结论SD大鼠胚胎视网膜内存在神经干细胞,并且可以进行体外培养和扩增。

基于神经团的视网膜神经系统建模研究

作为视觉系统最关键的部分,视网膜处于图像信息提取的前端,准确的视网膜模型对于完整的视觉系统建模至关重要。借鉴神经团理论,从集成的观点出发研究了视网膜建模问题,综合已有研究成果建立了较为完整的视网膜模型。建立的模型具有如下几方面特点:(1)在尺度上,从介观尺度上保证模型不同部分尺度的一致性;(2)在结构上,遵循视网膜的解剖结构,涵盖视网膜的主要部分,包括两个突触层和三个细胞层;(3)在神经元模型上,借鉴已有研究成果为不同神经元选择适合的神经元模型。针对建立的视网膜模型进行的分析表明:模型结构具有小世界网络特性,这与其他文献的分析结果是一致的;在动力学特性上,模型针对持续而固定的刺激呈现出稳定的类似极限环状态。

大鼠角膜穿通伤后局部应用IL-10抑制视网膜炎症和抗神经溃变的研究

目的:观察角膜穿通伤后局部应用IL-10对视网膜炎症反应的抑制和对神经溃变的保护作用。方法:将清洁级成年雌性SD大鼠50只,随机分为对照组(8只)、损伤组和治疗组,后两组(每组21只)再分为损伤1 d、2 d和3d组(每小组7只)。损伤组用无菌注射器刺穿眼球颞侧角膜缘角膜,制作角膜穿通伤模型。治疗组在角膜穿通伤后用IL-10溶液滴眼。各组2只大鼠用于制作眼球切片,免疫荧光染色观察角膜穿通伤后炎症因子IL-1β、IL-6和TNF-α以及神经丝蛋白-200(neurofilament protein-200,NF-200)、血影蛋白(α-Ⅱspectrin)及钙蛋白酶2(m-calpain)在视网膜中的分布特征;另5只大鼠用于提取视网膜蛋白,采用免疫印迹法检测各组大鼠于角膜穿通伤24,48,72 h后,视网膜组织内NF-200和血影蛋白降解产物以及活性钙蛋白酶2相对含量的动态变化。结果:对照组视网膜结构层次清楚,IL-1β、IL-6、TNF-α和m-calpain免疫荧光很弱;血影蛋白和NF-200免疫荧光染色可清晰显示阳性神经纤维;角膜穿通伤后,视网膜结构层次模糊,TNF-α、IL-1β,IL-6和m-calpain免疫荧光增强,主要分布在内层;NF-200和血影蛋白免疫荧光染色显示阳性神经纤维明显减少;IL-10治疗后,TNF-α、IL-1β,IL-6和m-calpain免疫荧光减弱,血影蛋白和NF-200阳性神经纤维明显多于损伤组。免疫印迹检测结果表明,损伤组视网膜组织内大分子的NF-200和血影蛋白含量逐渐减少,其小分子的降解产物以及小分子的活性m-calpain逐渐增加;在IL-10治疗组,NF-200和血影蛋白的降解产物以及活性m-calpain的增加程度明显减轻。结论:角膜穿通伤可刺激视网膜细胞高表达炎症因子IL-1β,IL-6和TNF-α,导致组织的炎症损伤,同时激活m-calpain,后者降解视网膜细胞骨架蛋白NF-200和血影蛋白,造成神经溃变;局部应用IL-10可减轻炎症反应,抑制m-calpain对骨架蛋白的降解,从而对视网膜细胞产生保护作用。