糖尿病视网膜病变/病理生理学

摘要： Metabolic memory means if the hyperglycemia can't be controlled at early stage of diabetes,chronic complications such as diabetic retinopathy (DR) will continue to develop even if the blood glucose level maintains normal level at later stage.Oxidative stress plays an important role in the "metabolic memory" of DR,which interacts with the nitrative stress,advanced glycation end products,genetic modification and endoplasmic reticulum stress in the pathogenesis of DR.Further elucidation of the relationship between oxidative stress and "metabolic memory" of DR can open the way for the discovery of novel therapeutic targets to prevent DR progression.%“代谢记忆”是指糖尿病患者的高血糖水平如果在发病早期不能得到及时控制,即使后期血糖持续稳定在正常水平,糖尿病视网膜病变(DR)等慢性并发症仍然会继续发展,难以逆转.氧化应激在DR的“代谢记忆”中起关键性作用.硝化应激、糖基化终末产物、炎症、表观遗传修饰及内质网应激相互作用,促进DR“代谢记忆”发生发展.深入研究氧化应激与DR“代谢记忆”之间的相关性,可为控制DR持续发展以及寻找新的治疗靶点提供思路.

摘要： Objective To observe the effect of different concentration netrin-1 on retinal vascular permeability in diabetes mellitus (DM) rats.Methods Eighty adult Sprague-Dawley rats were randomly divided into 8 groups,10 rats in each group,including normal control group (group A),normal+balanced salt solution (BSS) group (group B),normal+netrin-1 (500 μg/ml) group (group C) and DM group (50 rats in 5 subgroups).DM rats were induced by intraperitoneal injection of streptozocin.Three months after intraperitoneal injection,10 DM rats in the control group were injected with BSS (group D).Forty DM rats were injected with 5 μl of different concentrate netrin-1,and were divided into DM+netrin-1 10 μg/ml group (group E),DM+netrin-1 50 μg/ml group (group F),DM+netrin-1 100 μg/ml group (group G),DM+netrin-1 500 μg/ml group (group H)according to the different concentration.Non-DM rats in group C were injected with netrin-1 500 μg/ml.The expression of occludin was determined by immunohistochemistry for protein,and by real-time fluorescence quantitative reverse transcription polymerase chain reaction for mRNA level.Retinal vascular permeability was measured by Evans blue infusion.Results The expression of occludin protein and mRNA in group D were less than group A (t=27.71,8.59;P=0.00,0.00).However,the retinal vascular permeability increased in group D (t=-42.72,P=0.00).The expression of occluding protein,occludin mRNA and retinal vascular permeability showed significant differences between group D,E,F,G and H (F=146.31,16.54,67.77;P=0.00,0.00,0.00).Compared the group B with group C,there was no significant differences between the expression of occludin protein,occludin mRNA and the retinal vascular permeability (t=-1.13,0.93,1.04;P=0.27,0.36,0.31).The concentrate of netrin-1 showed a significant positive correlation to the expression level of occludin and occludin mRNA (r=0.73,0.81;P=0.00,0.00),but negative correlation to the vascular permeability (r=-0.61,P=0.00).Conclusion Netrin-1 can reduce the DM rats' retinal vascular permeability,which depended on the concentration of netrin-1.%目的 观察不同浓度外源性轴突导向因子(netrin)-1对糖尿病(DM)大鼠视网膜血管通透性的影响.方法 健康清洁级雄性Sprague-Dawley大鼠80只,采用随机数字表法随机分为正常对照组(A组)、正常+平衡盐溶液(BSS)组(B组)、正常+netrin-1 500 μg/ml组(C组)、DM+BSS组(D组)、DM+netrin-1 10 μg/ml组(E组)、DM+netrin-1 50 μg/ml组(F组)、DM+netrin-1 100 μg/ml组(G组)、DM+netrin-1 500 μg/ml组(H组),每组10只.E～H组大鼠腹腔注射链脲佐菌素诱导DM动物模型.建模3个月后,E～H组大鼠玻璃体腔分别注射10、50、100、500 μg/ml netrin-1 5μl.C组大鼠玻璃体腔注射500 μg/mlnetrin-1 5 ul.B、C组大鼠玻璃体腔注射等体积BSS.A组大鼠不做任何处理.采用免疫组织化学染色法观察大鼠视网膜闭合蛋白(occludin)的阳性表达;荧光定量聚合酶链反应检测大鼠视网膜occludin mRNA的表达;伊凡思蓝检测各组大鼠视网膜血管通透性变化.结果 与A组比较,D组大鼠视网膜occludin阳性表达(t=27.71,P=0.00)、mRNA表达(t=8.59,P=0.00)均减少,差异有统计学意义;视网膜血管通透性增加,差异有统计学意义(t=-42.72,P=0.00).D～H组大鼠视网膜occludin阳性表达(F=146.31,P=0.00)、mRNA表达(F=16.54,P=0.00)及视网膜血管通透性(F=67.77,P=0.00)比较,差异有统计学意义.B、C组大鼠视网膜occludin阳性表达(t=-1.13,P=0.27)、mRNA表达(t=0.93,P=0.36)及视网膜血管通透性(t=1.04,P=0.31)比较,差异无统计学意义.随着外源性netrin-1浓度升高,大鼠视网膜occludin阳性表达、mRNA表达升高,视网膜血管通透性降低.相关性分析结果显示,外源性netrin-1浓度与视网膜occludin阳性表达、mRNA表达呈正相关(r=0.73、0.81,P=0.00、0.00),与视网膜血管通透性呈负相关(r=-0.61,P=0.00).结论 外源性netrin-1可降低DM大鼠视网膜血管通透性,且该作用与外源性netrin-1浓度有关.

摘要： Objective To investigate the cellular viability and mitochondrial reactive oxygen species (ROS) production of the Müller cells under high glucose condition,and explore the protection role of the 5,6-dihydrocyclopenta-1,2-dithiole-3-thione (CPDT) on Müller cells.Methods Müller cells from Sprague Dawley rats were divided into 5 groups randomly,including 25 mmol/L normal glucose group (group A) and 65 mmol/L high glucose group (group B).High glucose group with 45,60,70 μmol/L CPDT and cultured them 72 hour was set as group C,D and E.Water soluble tetrazolium salt (WST)-8 was used to measure the cellular viability.Flow cytometry was used to measure the active oxygen and apoptosis index.The expression of nuclear factor erythroid 2-related factor 2 (Nrf2),hemeoxygenase-1 (HO-1),Bcl-2 and Bax protein were measured by Western blot.Results Compared with group A,the WST-8 showed that the viability of Müller cells apparently decreased in group B (t=39.59,P＜0.05).Compared with the group B,the viability of Müller cells had changes in group C (t=0.97,P＞0.05),but recovered in group D and E (t=-4.17,-7.52;P＜0.05).Compared with group A,the FCM showed that the mitochondrial ROS levels was higher in group B (t=-30.99,P＜0.05).Compared with group B,the mitochondrial ROS levels were decreased in group D (t=27.68,P＜0.05).Compared with group A,Bax,Nrf2 and HO-1 increased (t=-11.03,-63.17,-11.44;P＜0.05),while the bcl-2 decreased in group B (t=7.861,P＜0.05).Compared with the group B,Nrf2,HO-1 and Bax decreased (t=15.11,26.59,6.27;P＜0.05),while the bcl-2 increased in group D (t=-6.53,P＜0.05).Conclusions Under the high glucose,CPDT may reduce the mitochondrial ROS levels and the expression of Nrf2,HO-1 and Bax protein of Müller cells.It may inhibit apoptosis through activating the Nrf2/HO-1 pathway and balancing of level of Bcl-2 protein and mitochondrial ROS.%目的 观察5,6-二氢环戊烯1,2-二硫杂环戊烯-3-硫酮(CPDT)对高糖环境下大鼠视网膜Müller细胞活性及其线粒体活性氧(ROS)生成量的影响,初步探讨CPDT对高糖环境下Müller细胞的保护作用及其机制.方法 Sprague Dawley大鼠Müller细胞分为25 mmol/L对照组(A组)、65 mmol/L高糖(B糖)组、高糖+45 μmol/L CPDT组(C组)、高糖+60 μmol/L CPDT组(D组)、高糖+70 μmol/L CPDT组(E组).培养72 h后,水溶性四唑盐(WST)-8法检测各组Müller细胞的细胞相对增生率;流式细胞仪测定各组Müller细胞ROS生成量及细胞凋亡率;蛋白免疫印迹法(Western blot)测定Müller细胞中核因子-E2相关因子2(Nrf2)、血红素合晦-1 (HO-1)、B细胞淋巴瘤/白血病-2(Bcl-2)和Bcl相关X蛋白(Bax蛋白)表达的变化.结果 WST-8法检测结果显示,与A组比较,B组Müller细胞活性明显下降,差异有统计学意义(t=39.59,P＜0.05).与B组比较,C组Müller细胞活性无明显提高,差异无统计学意义(t=0.97,P＞0.05);D、E组Müller细胞活性恢复,差异有统计学意义(t=-4.67、-7.52,P＜0.05).流式细胞仪检测结果显示,与A组比较,B组Müller细胞中ROS生成量增加,差异有统计学意义(t=-30.99,P＜0.05);与B组比较,D组Müller细胞中ROS含量明显下降,差异有统计学意义(t=27.68,P＜0.05).Western blot检测结果显示,与A组比较,B组Müller细胞Bax、Nrf2、HO-1蛋白表达显著上调,差异有统计学意义(t=-1 1.03、-63.17、-11.44,P＜0.05);Bcl-2蛋白表达明显下调,差异有统计学意义(t=7.861,P＜0.05).与B组比较,D组Müller细胞Nrf2、HO-1、Bax蛋白表达均下调,差异有统计学意义(t=15.11、26.59、6.27,均P＜0.05);Bcl-2蛋白表达上调,差异有统计学意义(t=-6.53,P＜0.05). 结论 CPDT降低高糖环境下Müller细胞中ROS含量,下调Nrf2、HO-1、Bax蛋白表达;其机制与激活Nrf2/HO-1氧化应激通路,改变Bcl-2蛋白之间的平衡性,影响线粒体氧自由基量生成,从而抑制细胞凋亡有关.

摘要： Objective To observe the effect of netrin-1 on retinal Müller cells in diabetes mellitus (DM) rats. Methods Fifty Sprague-Dawley rats were randomly divided into the normal control group (group A), normal + balanced salt solution (BSS) group (group B), normal+netrin-1 group (group C), DM+BSS group (group D) and DM+netrin-1 group (group E), with 10 rats in each group. DM rats were induced by intraperitoneal injection of Streptozotocin (60 mg/kg). The expression level of glial fibrillary acidic protein (GFAP) on retinal Müller cells was determined by immunohistochemistry, the level of GFAP mRNA was analyzed by real-time fluorescence quantitative reverse transcription polymerase chain reaction. Results Immunohistochemistry showed that GFAP was distributed in retinal ganglion cells and retinal nerve fiber layer in group A, B and C. Compared to group B, GFAP staining was brighter in the group D. There were significant differences in the expression of GFAP protein and mRNA among groups A-E (F=203.43, 72.91; P=0.00, 0.00), they were higher in group D than group A (t=-26.01, 22.26; P=0.00, 0.00), and group E (t=-10.78, 3.93; P=0.00, 0.00). They were higher in group E than group A (t=7.00, -9.82; P=0.00,0.00). There were no significant differences in between group A and group C (t=-0.29, 0.50; P=0.77, 0.62). Conclusion The expression of GFAP in Müller cells of DM rats could be decreased by injecting netrin-1 into vitreous.%目的 观察外源性轴突导向因子-1(netrin-1)对糖尿病(DM)大鼠视网膜Müller细胞活化的影响.方法 健康清洁级雄性Sprague-Dawley大鼠50只,采用随机数字表法随机分为正常对照组(A组)、正常+平衡盐溶液(BSS)组(B组)、正常+netrin-1100μg/ml组(C组)、DM+BSS组(D组)、DM+netrin-1100μg/ml组(E组),每组10只.D、E组大鼠按60 mg/kg的剂量,左下腹腔注射链脲佐菌素诱导DM动物模型.采用免疫组织化学染色法检测大鼠视网膜Müller细胞标志物胶质原纤维酸性蛋白(GFAP)的阳性表达;荧光定量聚合酶链反应检测大鼠视网膜GFAP mRNA的表达.结果 免疫组织化学染色结果显示,A~C组大鼠视网膜仅在神经纤维层及神经节细胞层可见少量GFAP阳性表达.D组大鼠视网膜GFAP阳性表达增多.E组大鼠视网膜GFAP阳性表达较D组减少.A~E组大鼠视网膜GFAP阳性表达、mRNA表达比较,差异有统计学意义(F=203.43、72.91,P=0.00、0.00).与A组比较,D组大鼠视网膜GFAP阳性表达、mRNA表达明显增多,差异有统计学意义(t=-26.01、22.26,P=0.00、0.00).E组大鼠视网膜GFAP阳性表达、mRNA表达较D组明显下降(t=-10.78、3.93,P=0.00、0.00),但仍高于A组(t=7.00、-9.82,P=0.00、0.00),差异均有统计学意义.A、C组大鼠视网膜GFAP阳性表达、mRNA表达比较,差异均无统计学意义(t=-0.29、0.50,P=0.77、0.62).结论 Netrin-1可降低DM大鼠视网膜Müller细胞活化,减少视网膜GFAP表达.

摘要： 目的:探讨早期糖尿病视网膜病变(DR)状态下,缺氧诱导因子1αSymbolaA@_(HIF-1αSymbolaA@_)对血管内皮细胞表面细胞间粘附分子-1(ICAM-1)表达的影响.方法:收集早期DR患者及年龄匹配的健康人外周血血清,用于体外培养恒河猴视网膜血管内皮细胞系细胞(RF/6A).分为糖尿病血清培养组(B组)、糖尿病+HIF-1αSymbolaA@_反义寡核苷酸组(ASODN)(C组)、糖尿病+HIF-1αSymbolaA@_ 正义寡核苷酸组(SODN)(D组)健康人血清培养细胞为正常对照组(A组).使用免疫组织化学和免疫酶联吸附法(ELISA)检测HIF-1αSymbolaA@_和ICAM-1的表达水平.结果:在蛋白总量一致的情况下,A组细胞上清中sICAM-1的浓度为(13.89±1.35)ng/ml,而B组的浓度为(25.26±1.97)ng/ml ,HIF-1αSymbolaA@_ ASODN 转染可以明显降低细胞ICAM-1的表达水平,其浓度为(16.59±1.11)ng/ml,HIF-1αSymbolaA@_ SODN 转染则不能影响细胞ICAM-1的表达.各组细胞之间ICAM-1表达水平比较有统计学差异(F=81.89,P=0.00),各组之间两两比较,B组和D组之间比较无统计学差异(P=0.98),其余各组之间两两比较有统计学差异(P均<0.05). 结论:在体外培养条件下, HIF-1αSymbolaA@_对糖尿病血清培养条件下的RF/6A细胞表达ICAM-1具有调节作用.%Objective: To investigate the mediation of HIF-1 αSymbolaA@_ to the expression of ICAM-1 by retinal vascular endothelial cell under early stage of diabetic retinopathy condition.Methods:The rhesus choroid-retina vascular endothelial cell line RF/6A were cultured in RPMI 1640 medium-10% human serum, which was collected from the subjects of early stage of diabetic retinopathy and age-matched healthy control.The cells were cultured in 4 groups as control group(group A),diabetic group (group B), HIF-1 αSymbolaA@_ anti-sense oligonucleotides (ASODN) group (group C) and HIF-1 αSymbolaA@_ sense oligonucleotides (SODN) group (group D).ICAM-1 levels in RF/6A supernatants were determined with ELISA kit.Results: Contrast to group A, the level of ICAM-1 significantly increased in group B (25.26±1.97) ng/ml vs (13.89±1.35)ng/ml(P=0.00).But after HIF-1αSymbolaA@_ bioactivity was blocked (group C), the effect on the level of ICAM-1 by diabetic serum(group B) was suppressed significantly (25.26±1.97) ng/ml in group B(16.59±1.11) ng/ml in group C vs (25.26±1.97)ng/ml in group B(P=0.00).Conclusion: In vitro, HIF-1αSymbolaA@_ could regulate the expression of ICAM-1 by RF/6A.HIF-1αSymbolaA@_ may served as a therapeutic target for the treatment and/or prevention of early diabetic retinopathy.

摘要： Objective To evaluate the effect of FTY720 on retinal leukocytes adhesion and vascular permeability in diabetic retinopathy (DR) model,and explore its mechanism.Methods Ninety male Wister rats were randomly divided into normal control group,diabetic group and FTY720 group,thirty rats in each group.Diabetes was induced by giving a single intraperitoneal injection of streptozocin.FTY720 group was administered with FTY720 at a dose of 0.3 mg/kg by oral gavage daily for 3 months after establishment of diabetes.All rats were used for experiments following intervention for 3 months in FTY720 group.Immunohistochemical staining was used to observe the expression and distribution of intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1),and the positive cells were counted.Real-time reverse transcription PCR was used to measure mRNA expression of ICAM-1 and VCAM-1.Fluorescein isothiocyanate-Concanavalin A perfusion was used to detect retinal leukocytes adhesion.Evans blue (EB) perfusion was used to analyze retinal vascular permeability.Immunofluorescence staining was used to detect retinal inflammatory cells infiltration.Results In diabetic group,both ICAM-1(t =12.81) and VCAM-1 (t=11.75) positive cells as well as their mRNA expression (t=16.14,9.59) were increased compared with normal control group,with statistical significance (P＜ 0.05).In FTY720 group,both ICAM-1(t=-9.93) and VCAM-1 (t=-6.61) positive cells as well as their mRNA expression (t=-15.28,-6.10) were decreased compared with diabetic group,with statistical significance (P＜ 0.05).Retinal leukocytes adhesion (t=16.32) and EB permeability (t=17.83) were increased in diabetic group compared with normal control group,while they were decreased in FTY720 group compared with diabetic group(t=-9.93,-11.82),with statistical significance (P＜0.05).There were many CD45 positive leukocytes infiltration in retina of diabetic group,including CD11b positive macrophage/activated microglia,while both of them were little in FTY720 group.Conclusions FTY720 can decrease retinal leukocytes adhesion,reduce retinal vascular permeability and inflammatory cells infiltration,which is associated with down-regulation of ICAM-1 and VCAM-1.%目的 观察探讨FTY720对糖尿病大鼠视网膜血管内白细胞粘附和血管通透性的影响及机制.方法 雄性Wistar大鼠90只,随机分为正常对照组、糖尿病组和FTY720组,每组30只.糖尿病组和FTY720组大鼠采用一次性腹腔注射链脲佐菌素的方法建立糖尿病模型.建模成功后,FTY720组大鼠以0.3 mg/kg的剂量灌胃给予FTY720,1次/d,连续3个月.于FTY720组大鼠干预后3个月,3组大鼠均用于相关实验.采用免疫组织化学染色法观察大鼠视网膜细胞间粘附分子1(ICAM-1)和血管细胞粘附分子1(VCAM-1)的表达,并计数阳性细胞数;荧光定量逆转录聚合酶链反应(RT-PCR)检测大鼠视网膜ICAM-1、VCAM-1的mRNA表达;异硫氰酸荧光素标记的刀豆素蛋白灌注染色法检测大鼠视网膜血管内白细胞粘附情况;伊凡思蓝(EB)灌注染色法观察大鼠视网膜EB渗漏情况并定量;免疫荧光染色法检测视网膜炎性细胞浸润情况.结果 糖尿病组大鼠视网膜ICAM-1(t=12.81)、VCAM-1(t=11.75)阳性细胞数及ICAM-1(t=16.14)、VCAM-1(t=9.59)mRNA表达均较正常对照组明显增加,差异均有统计学意义(P＜0.05);FTY720组大鼠视网膜ICAM-1(t=-9.93)、VCAM-1(t=-6.61)阳性细胞数及ICAM-1(t =-15.28)、VCAM-1(t=一6.10)mRNA表达较糖尿病组明显减少,差异有统计学意义(P＜0.05).糖尿病组大鼠视网膜血管内粘附的白细胞计数(t=16.32)及平均EB渗漏量(t=17.83)较正常对照组明显增加,差异有统计学意义(P＜0.05);FTY720组大鼠视网膜血管内粘附的白细胞计数(t=-9.93)及平均EB渗漏量(t=-11.82)较糖尿病组明显减少,差异有统计学意义(P＜0.05).糖尿病组大鼠视网膜可见大量CD45阳性的白细胞浸润,其中CD11b阳性的巨噬细胞和(或)活化的小胶质细胞数量明显增多.FTY720组大鼠视网膜可见少量CD45阳性的白细胞浸润以及少量CD11b阳性的巨噬细胞和(或)活化的小胶质细胞.结论 FTY720可减少糖尿病大鼠视网膜血管内白细胞粘附,降低血管通透性.其机制可能与下调视网膜ICAM-1和VCAM-1的表达有关.

摘要： Diabetic retinopathy (DR) is a common cause of blindness,its occurrence and development are the synergic results of multiple factors.Current studies suggest that inflammation and inflammatory factor has an important role in the pathogenesis of DR.The occurrence and development of DR are closely related with interleukins,intercellular adhesion molecules,hasten factors,tumor necrosis factor,C-reactive protein etc.Mesenchymal stem cells (MSCs) are pluripotent cells derived from the mesoderm and have multiple differentiation potentials,and anti-inflammatory and immunosuppressive function.Recent studies shown that MSCs transplantation can protect damaged retina by inflammatory regulation,which become a new research direction for DR treatment.%糖尿病视网膜病变(DR)的发生发展是多因素协同作用的结果.目前研究认为炎症反应和炎性因子在DR发病机制中具有重要作用.白细胞介素、细胞间黏附分子、肿瘤坏死因子等炎性因子与DR的发生发展密切相关.间充质干细胞(MSCs)是来源于中胚层的多能干细胞,具有多潜能分化作用及抗炎和免疫抑制等功能.通过MSCs移植,发挥其炎症调节作用可为受损视网膜提供保护,成为DR治疗领域值得关注的研究方向.

摘要： 本发明涉及用于视网膜神经退行性疾病，特别是糖尿病视网膜病变的局部治疗和/或预防的肽，所述肽的序列长度为13‑50个氨基酸，所述肽的N‑端主要包含序列HXaa1EGTFTSDXaa2SXaa3Xaa4(SEQ ID NO：1)，其中：Xaa1是选自丙氨酸和甘氨酸的氨基酸；Xaa2是选自缬氨酸和亮氨酸的氨基酸；Xaa3是选自丝氨酸和赖氨酸的氨基酸；Xaa4是选自酪氨酸和谷氨酰胺的氨基酸；且组氨酸是N‑末端残基。本发明也包括用于这些疾病的局部治疗和/或预防的局部用药物组合物。

摘要： 本发明提供一种糖尿病及糖尿病视网膜病变网络防治系统，包括检测模块、读片智能诊断模块、信息存储模块和智能防治模块，所述检测模块包括血糖检测终端和眼底检测终端，用于检测患者的血糖浓度，并为患者拍摄眼底影像图片，所述读片智能诊断模块包括读片单元和智能诊断单元，用于对眼底影像图片提供专业的读片结果和诊断结果，所述无线传输模块用于传输血糖浓度信息及眼底影像图片，所述信息存储模块用于存储血糖信息和眼底影像图片，所述智能防治模块包括糖尿病防治单元、糖尿病视网膜病变防治单元和用户终端，用于为患者提供治疗方案。以解决信息录入繁琐、消耗人力及时间，以及对视网膜病变照片诊断不够全面等问题。

摘要： 本发明涉及一种药物的新用途，具体地说是青藤碱在治疗增龄性黄斑变性(Age-relatedmaculardegeneration)、视网膜色素变性(pigmentarydegenerationoftheretina)和糖尿病视网膜病变(diabeticretinopathy)等疾病中的应用，本发明人研究证明青藤碱都可以发挥到很好的治疗作用。

摘要： 本发明涉及用于视网膜神经退行性疾病，特别是糖尿病视网膜病变的局部治疗和/或预防的肽，所述肽的序列长度为13-50个氨基酸，所述肽的N-端主要包含序列HXaa1EGTFTSDXaa2SXaa3Xaa4(SEQ？ID？NO：1)，其中：Xaa1是选自丙氨酸和甘氨酸的氨基酸；Xaa2是选自缬氨酸和亮氨酸的氨基酸；Xaa3是选自丝氨酸和赖氨酸的氨基酸；Xaa4是选自酪氨酸和谷氨酰胺的氨基酸；且组氨酸是N-末端残基。本发明也包括用于这些疾病的局部治疗和/或预防的局部用药物组合物。

摘要： 本发明提供了治疗眼部新血管形成、血管发生、视网膜水肿、糖尿病视网膜病变和/或视网膜缺血的组合物和方法，以预防与这类病症相关的视力损失。更具体地，本发明提供了含有独特结合特性的受体酪氨酸激酶(RTK)抑制剂的组合物以及它们在治疗眼部障碍中的用途。

摘要： 本发明提供了治疗眼部新血管形成、血管发生、视网膜水肿、糖尿病视网膜病变和/或视网膜缺血的组合物和方法，以预防与这类病症相关的视力损失。更具体地，本发明提供了含有独特结合特性的受体酪氨酸激酶(RTK)抑制剂的组合物以及它们在治疗眼部障碍中的用途。

摘要： 本发明提供一种糖尿病及糖尿病视网膜病变网络防治系统，包括检测模块、读片智能诊断模块、信息存储模块和智能防治模块，所述检测模块包括血糖检测终端和眼底检测终端，用于检测患者的血糖浓度，并为患者拍摄眼底影像图片，所述读片智能诊断模块包括读片单元和智能诊断单元，用于对眼底影像图片提供专业的读片结果和诊断结果，所述无线传输模块用于传输血糖浓度信息及眼底影像图片，所述信息存储模块用于存储血糖信息和眼底影像图片，所述智能防治模块包括糖尿病防治单元、糖尿病视网膜病变防治单元和用户终端，用于为患者提供治疗方案。以解决信息录入繁琐、消耗人力及时间，以及对视网膜病变照片诊断不够全面等问题。

摘要： 本发明公开了稳定和组织视网膜组织，尤其是布鲁赫膜(Bruch’s membranes)的细胞外基质中的胶原原纤维的方法，以及稳定衬有布鲁赫膜的视网膜色素上皮层的方法。所述稳定化作用和组织化作用可以通过用交联和组织胶原原纤维的蛋白质，如核心蛋白聚糖(decorin)，治疗视网膜组织来实现。稳定化和组织化方法包括：在诊断干性黄斑变性、诊断早期糖尿病性视网膜病变和早期糖尿病性黄斑水肿之前、期间或之后对视网膜组织进行治疗，以预防、延缓或限制布鲁赫膜和衬有布鲁赫膜的视网膜色素上皮细胞解组织的进程。

摘要： 本发明公开了一种糖尿病视网膜病变全视网膜体外培养模型的构建方法，属于动物疾病模型领域。本发明的模型构建方法是将大鼠或胚胎猪视网膜置入含D‑葡萄糖、Neurobasal A、N2/B27 supplement、胰岛素、BSA、cpt‑cAMP的DMEM/F12培养液培养即可。本发明的方法可以快速得到具有典型糖尿病视网膜病变症状的体外模型，耗时短，可重复，应用价值良好。

摘要： 本发明涉及基于可解释性病变植入的糖尿病性视网膜病变检测方法，基于可解释性病变植入的糖尿病性视网膜病变检测方法：首先获取相关IDRID的数据集，对数据集进行预处理，裁剪为512x512的尺寸，使用UNet改进结构同时引入高斯函数和opencv库，提取出病变的信息，得到存取病变信息的病理描述符，然后使用Encoder‑Decoder+Transformer+CodeBook结构生成含有病变的高分辨率视网膜血管图，再基于Pix2PixHD模型实现风格迁移，生成最终的糖尿病视网膜图，最后将增强的数据集在分类器中进行训练和测试。