姜黄素对高糖诱导的人视网膜血管内皮细胞增殖及VEGF和NF-κB p65表达的抑制作用

目的：观察不同浓度姜黄素对体外高糖诱导的人视网膜血管内皮细胞(HRCECs)增殖及血管内皮生长因子(VEGF)、核因子-κB(NF-κB)p65表达的影响。

方法：用高糖培养基模拟糖尿病环境建立HRCECs体外高糖模型,将培养的细胞分为：正常对照组、高糖对照组、高糖+20、40、80μmol/L姜黄素组,分别用CCK-8法检测姜黄素干预后HRCECs的增殖能力,用Western-blot及免疫细胞化学法检测VEGF、NF-κB p65的表达。

结果：CCK-8法结果示：与正常对照组比较,高糖显著促进HRCECs增殖(P<0.01),各浓度姜黄素作用12、24、48h后与高糖对照组比较,细胞增殖均有明显抑制作用(P<0.01),且呈浓度与时间依赖性。Western-blot结果示：与正常对照组比较,高糖对照组中VEGF-A、NF-κB p65表达显著增加(P<0.01),各浓度姜黄素作用12、24、48h后与高糖对照组比较,VEGF-A、NF-κB p65的表达显著减少,且随着浓度增加、时间延长抑制作用增强,各加药组间两两比较均有差异(P<0.01)。免疫细胞化学法结果示：与正常对照组相比,高糖对照组VEGF表达显著增加(P<0.01),各浓度姜黄素干预24h后与高糖对照组比较,VEGF表达逐渐下降(P<0.01),各加药组间两两比较均有差异(P<0.01)。

结论：姜黄素可呈浓度与时间依赖性地抑制高糖诱导的HRCECs增殖以及VEGF、NF-κB p65的表达,这种增殖抑制作用可能与其下调VEGF、NF-κB p65表达有关。     

薏苡仁油对高糖环境下人视网膜血管内皮细胞增殖和VEGF表达的影响

目的:研究不同浓度的薏苡仁油对体外高糖条件下培养的人视网膜血管内皮细胞(HRCECs)增殖及血管内皮生长因子(VEGF)表达的影响。方法:将新鲜人眼球提取的HRCECs进行体外培养,最终用于实验的为生长良好的第3~4代细胞,实验分为空白对照组、低糖对照组、高糖对照组,高糖+不同浓度(50μL/mL,100μL/mL,200μL/mL)薏苡仁油组。不同浓度的薏苡仁油对体外培养的HRCECs增殖的抑制作用是通过用噻唑蓝比色法(MTT)检测。各分组HRCECs中VEGF的表达由免疫细胞化学法检测。结果:MTT比色法结果显示:不同浓度的薏苡仁油作用于体外培养的HRCECs 48h,其细胞增殖抑制与高糖对照组相比有显著性差异(P<0.05)。48h内呈浓度依赖性。而低糖对照组与高糖对照组差异无统计学差异(P>0.05)。免疫细胞化学检测法表明:用50,100,200μL/mL的薏苡仁油作用于高糖下HRCECs 48h,高糖+不同浓度薏苡仁油组与高糖对照组相比VEGF表达下降明显(P<0.05),将高糖+不同浓度薏苡仁油组之间进行两两比较亦具有统计学意义(P<0.05)。且呈浓度依赖性。高糖对照组与低糖对照组相比,VEGF表达明显(P<0.05)。结论:薏苡仁油可抑制高糖环境下HRCECs的增殖和VEGF的表达。     

青蒿琥酯对高糖环境下人视网膜微血管内皮细胞增殖及VEGF表达的影响

目的:研究青蒿琥酯(artesunate)对体外高糖环境下培养的人视网膜微血管内皮细胞(human retinal capillary endothelialcells,HRCECs)的增殖及血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)表达的影响。方法:从新鲜人眼球提取HRCECs,进行体外培养。取第3～4代生长良好的细胞用于实验,实验分为低糖对照组、高糖对照组、高糖+不同浓度青蒿琥酯组(15,30,60,120μg/mL),用噻唑蓝(MTT)比色法检测HRCECs的增殖,通过免疫细胞化学法观察各分组HRCECs中VEGF的表达。结果:MTT比色法检测细胞增殖结果显示:与低糖组比较,高糖显著促进HRCECs增殖(P>0.05);15,30,60,120μg/mL青蒿琥酯处理24h或48h,可时间和浓度依赖性地抑制高糖环境下HRCECs的增殖(P<0.05)。免疫细胞化学法检测VEGF表达结果显示:与低糖对照组相比,高糖对照组VEGF表达明显增加(P<0.05);高糖+不同浓度青蒿琥酯(15,30,60μg/mL)组与高糖对照组相比VEGF表达明显下降(P<0.05),高糖+不同浓度青蒿琥酯组之间两两比较均具有统计学差异(P<0.05),且随着药物浓度的提高,VEGF的表达量逐渐减少。结论:青蒿琥酯呈浓度依赖性地抑制高糖环境下HRCECs的增殖以及VEGF的表达,表明青蒿琥酯抑制高糖环境诱导HRCECs增殖可能与其抑制VEGF表达有关。     

银杏叶提取物对高糖环境下人视网膜血管内皮细胞增殖、凋亡的影响

目的:研究不同浓度的银杏叶提取物(ginkgo biloba ex-tract,GBE)对体外培养的高糖环境下人视网膜微血管内皮细胞(human retinal capillary endothelial cells,HRCECs)增殖和凋亡的影响。方法:体外培养从角膜移植术后新鲜人眼球提取的HRCECs。取生长良好的第3～4代细胞用于实验,实验分为低糖对照组、高糖对照组、高糖+不同浓度GBE组,用噻唑蓝(MTT)比色法检测HRCECs的增殖。吖啶橙(AO)/溴乙锭(EB)荧光双染色、流式细胞术检测HRCECs的凋亡率,并在荧光显微镜下观察荧光染色后HRCECs凋亡形态学改变。结果:MTT比色法结果显示:用12.5,25.0,50.0,100.0mg/L的GBE处理高糖环境下HRCECs,作用24,48,72h,高糖+不同浓度GBE组与高糖对照组相比具有显著性差异(P<0.05),高糖+不同浓度GBE组之间两两比较均具有显著性差异(P<0.05)。AO/EB荧光染色法、流式细胞术检测细胞凋亡率显示:高糖+不同浓度GBE组与高糖对照组比较均有显著性差异(P<0.05),高糖对照组显著高于低糖对照组(P<0.05)。荧光显微镜下观察到活细胞,早期凋亡细胞,晚期凋亡细胞,非凋亡的死亡细胞生物学形态改变的特征。结论:GBE促进高糖环境下HRCECs的增殖,抑制其凋亡。     

人参皂苷Rg3对高糖下视网膜血管内皮细胞增殖及ICAM-1表达的影响

目的:研究人参皂苷Rg3对体外培养的高糖条件下人视网膜血管内皮细胞(human retinal capillary endothelial cell,HRCEC)增殖与细胞间黏附分子-1(intercellular adhesionmolecule-1,ICAM-1)表达的影响。方法:体外培养从角膜移植术后新鲜人眼球提取的HRCECs。取生长良好的第3~4代细胞用于实验,实验分为低糖对照组、高糖对照组、高糖+不同浓度Rg3组,用噻唑蓝(MTT)比色法检测HRCEC的增殖。通过免疫细胞化学法观察各分组HRCEC ICAM-1的表达情况。结果:MTT比色法结果显示,高糖对照组与低糖对照组没有显著差异(P>0.05),用10,20,40,80,160mg/L的人参皂苷Rg3处理高糖下HRCEC24,48,72h与高糖对照组相比具有显著性差异(P<0.05),高糖+不同浓度Rg3组之间呈时间和浓度的显著性差异(P<0.05)。免疫细胞化学检测显示,与低糖对照组相比,高糖对照组ICAM-1表达明显(P<0.05),用40,80,160mg/L的人参皂苷Rg3处理高糖下HRCEC48h与高糖对照组相比ICAM-1表达有显著性差异(P<0.05),高糖+不同浓度Rg3组之间两两比较均具有显著性差异(P<0.05)。结论:人参皂苷Rg3可抑制高糖下视网膜血管内皮细胞增殖和ICAM-1表达。     

白藜芦醇对高糖环境下视网膜血管内皮细胞增殖及HMGB1乙酰化的影响

目的：探讨白藜芦醇对高糖环境下视网膜血管内皮细胞增殖的影响,并对其机制进行探讨。

方法：人视网膜血管内皮细胞培养于低糖或高糖环境,通过MTT法测定各组细胞增殖,研究白藜芦醇对高糖培养的视网膜血管内皮细胞增殖的影响。通过Western-blot及免疫共沉淀检测SIRT1表达及HMGB1的乙酰化。

结果：白藜芦醇对高糖环境下的视网膜血管内皮细胞增殖具有显著抑制作用(P<0.05),且随白藜芦醇剂量增加,抑制作用增强。高糖抑制SIRT1表达,提高HMGB1的乙酰化,白藜芦醇能逆转上述改变。

结论：白藜芦醇可能通过SIRT1-HMGB1通路抑制高糖环境下的视网膜血管内皮细胞增殖。     

胃饥饿素对高糖下人视网膜血管内皮细胞的保护作用及机制

目的：探讨胃饥饿素(ghrelin)对高糖下的人视网膜血管内皮细胞的保护作用及机制。

方法：以人视网膜血管内皮细胞为研究对象,建立高糖损伤模型。胃饥饿素处理细胞后,采用CCK-8试剂盒检测不同浓度胃饥饿素对高糖下细胞增殖的影响,以筛选最佳浓度。将细胞分为正常对照组(NC)、胃饥饿素组(ghrelin)、高糖组(HG)和胃饥饿素+高糖组(ghrelin+HG)。采用CCK-8试剂盒检测细胞增殖,Annexin-APC/7-AAD试剂盒检测细胞凋亡,蛋白质印迹法检测细胞NLRP3、Caspase-1、IL-1β及IL-18的表达。

结果：与NC组(100.00%±0.00%)相比,HG组细胞增殖率(69.87%±0.68%,P<0.05)明显下降。与HG组相比,ghrelin+HG组细胞增殖率(92.31%±3.62%,P<0.05)明显升高。与NC组(4.94%±0.15%)相比,HG组细胞凋亡率(28.33%±1.37%,P<0.05)明显升高。与HG组相比,ghrelin+HG组细胞凋亡率(14.24%±0.32%,P<0.05)明显降低。与NC组相比,HG组细胞表达NLRP3、Caspase-1、IL-1β及IL-18蛋白均明显升高(均P<0.05)。与HG组相比,ghrelin+HG组细胞表达NLRP3、Caspase-1、IL-1β及IL-18蛋白均明显下降(均P<0.05)。

结论：胃饥饿素能对高糖损伤的视网膜血管内皮细胞起到保护作用,可能是通过抑制NLRP3炎症小体信号通路发挥其功能。     

P97抵抗高糖培养的人视网膜血管内皮细胞增殖

目的:研究含缬酪肽蛋白(valosin-containing protein,P97)对高糖培养的人视网膜血管内皮细胞的作用。方法:体外高糖培养人视网膜血管内皮细胞(HRCECs),转染P97的RNA干扰质粒到HRCECs,抑制P97的表达,观察血管内皮生长因子(VEGF)的mRNA水平变化,同时观察HRCECs增殖的变化。结果:RNA干扰P97组和对照组的VEGF/actin分别为:0.21±0.03和0.10±0.01,两组差异有显著性(P<0.05),RNA干扰P97组和对照组,HRCECs在G1期细胞分别为44.05%±3.62%、25.21%±3.20%,两组比较差异有显著性(P<0.05)。结论:当P97表达受抑制后,VEGF的表达增高,HRCECs的增殖增强,这些变化可能与DR的发生发展相关。     

阿魏酸钠对高糖环境下人视网膜内皮细胞表达的影响

目的:研究体外环境下高糖培养的人视网膜血管内皮细胞(human retinal capillary endothelial cells,HRCEC)经过不同浓度的阿魏酸钠(sodium ferulate,SF)作用后的增殖以及血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)表达的影响。方法:对眼科手术新鲜的人角膜移植术后眼球进行取材并进行HRCEC的原代培养。进行实验的为生长良好的第3～4代细胞,实验分为空白对照组、低糖对照组、高糖对照组、高糖+不同浓度阿魏酸(1mg/L,2mg/L,3mg/L,4mg/L)组,用噻唑蓝比色法(MTT)检测48h后不同浓度的阿魏酸钠对其增殖的抑制作用。免疫细胞化学法用于检测低糖对照组、高糖对照组和不同浓度阿魏酸(1mg/L,2mg/L,4mg/L)组HRCEC中VEGF的表达。结果:MTT比色法结果表明:48h后不同浓度的阿魏酸钠分别作用于原代培养的HRCEC细胞增生抑制率分别为46.97%,61.55%,76.91%和83.47%。一定质量浓度范围内阿魏酸钠对高糖环境下HRCEC具有明显的增殖抑制作用(P<0.05)。低糖对照组与高糖对照组吸光度A结果相比,差异无统计学意义(P=0.068>0.05)。低糖对照组、高糖对照组与浓度分别为1mg/L,2mg/L,4mg/L的阿魏酸钠作用组作用于HRCEC 48h后免疫细胞化学背景灰度值与阳性灰度值之差分别为28.27±1.62,93.67±0.81,72.67±2.89,53.73±1.70,30.93±3.72。通过48h后加药组和高糖对照组相比,VEGF表达下降明显,且均有统计学意义(均为P<0.05),具有质量浓度依赖性。与低糖对照组相比,高糖对照组VEGF的表达明显增加(P<0.05)。结论:阿魏酸钠对体外培养的高糖环境下HRCEC的增殖及高糖引起VEGF表达具有抑制作用。     

高糖环境下内脏脂肪素在人视网膜色素上皮细胞中的作用

目的：观察体外高糖诱导环境,对人视网膜色素上皮细胞中内脏脂肪素(Visfatin)的表达影响,以及研究高糖环境下重楼皂苷I(Polyphyllin I)对Visfatin表达情况的影响。

方法：人视网膜色素上皮细胞培养后分3组,正常对照组、高糖组和高糖加Polyphyllin I药物干预组,干预培养12h后进行检测。正常对照组：5.5mmol/L葡萄糖浓度常规培养; 高糖组：将25mmol/L的高糖加入培养基建立模型; 高糖加Polyphyllin I药物干预组：高糖25mmol/L和3μg/L Polyphyllin I药物加入培养基。免疫荧光染色法观察人视网膜色素上皮细胞中Visfatin和血管内皮细胞生长因子(VEGF)表达; 实时荧光定量PCR检测上皮细胞中Visfatin和VEGF mRNA的表达; Western-blot法检测上皮细胞中Visfatin和VEGF蛋白的表达。

结果：免疫荧光检测发现Visfatin和VEGF在正常组视网膜色素上皮细胞中表达呈弱阳性。但在高糖组视网膜色素上皮中可见Visfatin和VEGF呈强阳性表达。药物干预组中Visfatin和VEGF荧光较高糖组明显减弱。RT-PCR显示高糖组Visfatin mRNA表达水平较正常组和干预组明显增高(t=4.24、3.89,均P<0.05)。高糖组VEGF mRNA表达水平较正常组和干预组明显增高(t=3.53、2.57,均P<0.05)。Western-blot结果示Visfatin蛋白水平,高葡萄糖组表达量显著高于正常对照组(t=3.62,P=0.01),干预组表达低于高糖组(t=3.79,P<0.01)。

结论：高糖环境可刺激视网膜色素上皮细胞中Visfatin的表达增加,Polyphyllin I可抑制高糖环境下视网膜色素上皮细胞中Visfatin的表达,可能为治疗糖尿病视网膜病变提供新的思路。     

A review of techniques and outcomes of endothelial keratoplasty in congenital hereditary endothelial dystrophy

Congenital hereditary endothelial dystrophy affects the Descemet membrane and endothelium, resulting in corneal decompensation. Penetrating keratoplasty (PKP) has been the gold-standard surgical management until recently; however, at present, endothelial keratoplasty (DSEK/DSAEK/n-DSEK: Descemet-stripping or non-Descemet stripping endothelial keratoplasty and DMEK/n-DMEK: Descemet membrane endothelial keratoplasty) is being preferred due to lesser intraoperative and postoperative complications, early visual recovery, and comparable visual outcomes. Endothelial keratoplasty (EK) can be challenging, especially in pediatric eyes with CHED due to smaller eyeballs, shallow anterior chambers, phakic status, and poor intraoperative visibility due to thick and hazy corneas. A total of 198 articles matched our search strategy. After screening for duplication and going through the titles and abstracts, 12 relevant original articles, one case series, and six case reports were included in this review. Various surgical modifications have to be adopted in comparison to adult eyes to overcome the aforementioned difficulties. Regardless, studies have shown favorable visual outcomes with better graft survival and fewer complications in eyes that underwent EK compared to PKP. Hence, timely surgical intervention and strict amblyopia management can result in better final visual outcomes. The purpose of this review is to summarize various intraoperative difficulties and the surgical modifications required, different surgical techniques, visual and graft-related outcomes, and various complications of EK in CHED eyes.     

Clinical results of non-Descemet stripping endothelial keratoplasty

AIM: To investigate the impact of non-Descemet stripping endothelial keratoplasty (non-DSEK) on graft rejection rate, and its overall procedural effectiveness in patients. METHODS: Non-DSEK was performed on 65 eyes of 64 patients, and the procedural outcomes, including rejection episodes, failure and dislocation of the grafts, best corrected visual acuity (BCVA), endothelial cell density (ECD), and other complications, were analyzed retrospectively. RESULTS: Of the 65 eyes, 63 recovered from bullous keratopathy with a clear cornea. The mean follow-up time was 26.4mo (range, 6-84mo). The mean BCVA improved from 1.70 logMAR preoperatively to 0.54 logMAR at 3mo, 0.46 logMAR at 6mo, and 0.37 logMAR at 1y after surgery. The postoperative donor ECD of the 25 patients who successfully underwent specular microscopic examination was 1918±534 cells/mm2 (range, 637 to 3056 cells/mm2), and the mean endothelial cell loss was 41.9% at 24mo postoperatively. One eye developed secondary glaucoma and required regrafting via penetrating keratoplasty (PKP). Another eye had postoperative graft failure due to rejection at 26mo. Postoperative graft dislocation occurred in eight eyes. All of the eight dislocated grafts were reattached using air reinjection. CONCLUSION: Immunological graft rejection of the donor graft rarely occurs in non-DSEK. Therefore, non-DSEK is a safe, concise, and effective alternative to restore corneal decompensation when the Descemet membrane is disease-free.     

One-Year Observation of Transplanted Human Corneal Endothelium

In 34 penetrating corneal transplants, endothelial photographs were taken preoperatively and at four postoperative intervals: four days, three weeks, three months, and one year. Preoperative corneas from older donors had larger and more variably sized endothelial cells. Although the mean endothelial cell loss at the four day examination was only 17%, it continued at a linear rate so that by one year almost half of the central endothelial cells were gone. The continued cell loss was not significantly affected by the operative cell loss, the presence of a lens postoperatively, or the recipient endothelial status. Six of the 34 transplants sustained documented episodes of allograft rejection, but their endothelial cell losses were minimized by prompt treatment with corticosteroids. The cell losses in the 20 phakic and 14 aphakic transplants were similar at both the four-day and one-year intervals, although the aphakic grafts were thicker at both times. Two additional transplants with vitreous touch to the graft endothelium sustained large continuing endothelial cell losses despite maintenance of clear, thin transplants.     

Comparison of penetrating and endothelial keratoplasty in patients with iridocorneal endothelial syndrome: A registry study

Background

To compare graft survival of endothelial keratoplasty (EK) versus penetrating keratoplasty (PK) in patients with iridocorneal endothelial (ICE) syndrome and identify ocular features associated with graft survival.

Methods

Observational, prospective, cohort study. A total of 30 806 first grafts performed between 1985 and 2020 were identified through the Australian Corneal Graft Registry and included in this observational, prospective cohort study. A total of 196 eyes underwent a primary corneal graft for ICE syndrome. Kaplan–Meier graft survival plots and Chi-squared tests were performed to identify graft survival rates for EK and PK. A history of raised intraocular pressure (IOP) was also recorded and analysed. Graft survival of eyes with ICE syndrome were compared to that of other indications.

Results

Grafts performed for ICE syndrome increased to 0.8% of all cases during the 2005 to 2020 period compared with 0.5% between 1985 to 2004 (χ²=9.35, p = 0.002). From 2010, EK surpassed PK as the preferred graft type. Survival of primary grafts in eyes with ICE syndrome was lower than for other indications (log-rank = 56.62, p < 0.001). Graft survival was higher following PK than Descemet stripping (automated) endothelial keratoplasty (DS(A)EK) (log-rank = 10.56, p = 0.001). Graft survival was higher in eyes without a history of raised IOP compared to those with a reported history of raised IOP (log-rank = 13.06, p < 0.001).

Conclusions

ICE syndrome carries a poor prognosis for graft survival. DS(A)EK had a poorer prognosis than PK. A history of raised IOP is associated with higher risk of graft failure.     

Culture and identification of endothelial progenitor cells from human umbilical cord blood

AIM: To elucidate a simple method for isolating endothelial progenitor cells (EPCs) from human umbilical cord blood mononuclear cells and observe the endothelial cell-specific expression profile during proliferation and differentiation in vitro. · METHODS: Human umbilical cord blood were isolated by Percoll density gradient centrifugation from human cord blood and cultured in vitro. The adherent cells were then identified by immunohistochemical staining and flow cytometric analysis. CD34, vascular endothelial growth factor receptor-2 (VEGFR-2), EPCs specific antigen CD133, as well as endothelial cell specific markers CD31 and vWF were used. The cells were characterized by acetylated LDL(acLDL) up-taking and lectin binding by direct fluorescentstaining. · RESULTS: During culture, the attached cells exhibited spindle-shape in early stage, and gradually display endothelium- like cobblestone morphology with outgrowth. On day 7, flow cytometric analysis showed that the positive staining rate of attached cells for CD133, CD34 and VEGFR-2 were 17.8%±3.7%, 22.1%±4.4% and 81.5%±5.0%, respectively. While, immunohistochemical staining showed that the adherent cells were positive to CD31 and vWF at the rate of 92.7%±2.2% and 73.3%±4.2%, respectively. By direct fluorescentstaining, we observed that 83.0%±4.3% of the attached cells were double positive for DiI-acLDL and FITC-UEA-I. · CONCLUSION: EPCs can be separated from human cord blood under certain conditions in vitro. This observation may provide a basis for study of relationship between EPCs and retinal neovascularization, as well as further clinical application of EPCs in ischemic retinal lesions.     

人脐血内皮祖细胞体外培养和鉴定的研究(英文)

目的:阐述从人脐血单核细胞分离培养EPCs的方法,并观察EPCs体外增殖分化过程中内皮细胞特异性抗原的表达,为进一步研究EPCs在缺血性视网膜疾病的临床应用奠定基础。方法:采用密度梯度离心方法获得脐带血单个核细胞,体外进行诱导、分化和扩增,通过免疫组化和流式细胞仪分析等技术对脐血来源的EPCs进行鉴定,在我们的研究中主要分析CD34,血管内皮细胞生长因子受体-2(VEGFR-2),EPCs特异性抗原CD133,以及内皮细胞特异性抗原CD31和第八因子相关抗原(vWF)的表达情况。同时我们通过分析细胞摄取乙酰化低密度脂蛋白(acLDL)和结合植物凝集素的能力进一步鉴定细胞。结果:脐带血单个核细胞在培养早期主要为梭形细胞,逐渐呈现铺路石样外观;在细胞培养至第7d,贴壁细胞流式细胞仪分析显示,CD133, CD34和VEGFR-2的阳性率分别为17.8%±3.7%, 22.1%±4.4%和81.5%±5.0% ;免疫组化染色结果显示CD31、vWF的表达率分别为92.7%±2.2%和73.3%±4.2%;免疫荧光染色结果表明83.0%±4.3%的贴壁细胞DiI-acLDL和FITC-UEA-I染色均阳性。结论:本实验证明在体外特定的培养条件可以从脐带血单个核细胞中分离培养出EPCs,为进一步研究EPCs与视网膜新生血管的关系以及EPCs治疗缺血性眼底的临床研究奠定了基础。     

后弹力层角膜内皮移植术应用与手术技术

角膜内皮移植(endothelial keratoplasty,EK)是针对内皮细胞功能障碍的靶向性治疗方法.目前已成为国际上治疗角膜内皮病变的首选方法.而后弹力层角膜内皮移植术(Descemet's membrane endothelial keratoplasty,DMEK)是目前EK最新技术,也称为小切口角膜内皮移植术,从解剖学角度完美恢复了角膜组织的正常结构,可更好更快恢复视力,且术后排斥反应显著降低,受到了广泛关注和认可.然而,DMEK作为一项新技术,虽然具有显著的优点,也面临着技术上的挑战.最受关注的是供体制备过程中内皮片的丢失、植入受体的展开和位置调整.目前随着手术方法和设备的不断改进,植入技术不断改进,学习曲线正在逐渐减低,越来越多的眼科医生掌握了该技术.由于角膜材料与手术适应证等限制,目前我国尚无开展DMEK的报道.     

角膜后弹力膜内皮移植术研究进展

角膜后弹力膜内皮移植术由于具有相对较低的移植排斥率以及较好的视力预后等优势,目前已成为部分发达国家治疗角膜内皮失代偿的主流手术方式,但限于手术难度较高,学习曲线较长,中国人前房偏浅,加之国内角膜内皮病变往往合并有其他较复杂的眼部疾病,目前国内尚未普遍开展这一手术。本文就角膜后弹力膜内皮移植术的手术适应证、供体植片制备(...     

利用后弹力层撕除术建立兔眼角膜内皮失代偿模型的评估

目的利用后弹力层撕除术建立一种新的角膜内皮失代偿模型以便更好地了解该手术的组织反应。方法根据手术方法的不同将40只新西兰成年兔平均分为4组：角膜内皮刮除组、后弹力层撕除组、后弹力层撕除角膜内皮移植术（DSEK）组及DSEK供体组;右眼为手术眼。每组定期通过角膜内皮活体染色,眼前节照相和UBM至少观察2个月。结果后弹力层撕除组角膜始终保持混浊,角膜内皮刮除组和DSEK组角膜逐渐透明,角膜厚度逐渐降低。活体染色显示角膜后弹力层撕除组术后2个月仍无角膜内皮生长。结论后弹力层撕除术建立的角膜内皮失代偿模型显示了后弹力层撕除后角膜内皮愈合过程,可用于角膜内皮移植的研究。     

角膜内皮移植技术的发展

角膜内皮移植术已成为治疗各种原因引起的角膜内皮功能失代偿的首选术式.角膜内皮移植手术与穿透性角膜移植手术相比,其较好地保持了眼前节的生物学完整性,术后视力恢复更快、更好,大大降低术后并发症等.本文就角膜内皮移植技术的发展过程,主要手术方式,手术的优缺点及术后并发症等进行综述,以期为临床应用提供参考.