视中枢提取液对体外培养的视网膜组织的一氧化氮及其合成酶的影响

目的：观察不同成分的培养液对成年犬体外培养的视网膜组织的NO及其合成酶的影响,旨在为视网膜移植提供抗氧化能力的保护性方法。方法：健康成年家犬31只（62眼）,将动物随机分成6组,I（新鲜视网膜组）、Ⅱ（常规培养液组）、Ⅲ（高浓度视中枢提取液组）、Ⅳ（低浓度视中枢提取液组）、Ⅴ（高浓度全脑组织提取液组）、Ⅵ（低浓度全脑组织提取液组）,将各组视网膜组织块放入相应培养基中培养一周。6组视网膜取材后进行NO、NOS生化指标的测定。结果：I-Ⅵ组视网膜组织NO、NOS含量差异有显著性,与I组相比,Ⅱ、Ⅲ、Ⅴ、Ⅵ组NO、NOS值显著增高;与Ⅱ组相比,Ⅲ、Ⅳ组NO、NOS值显著降低;且Ⅳ组与I组NO值统计学差异无显著性意义。Ⅳ组与Ⅲ组比较,NOS值降低明显。结论：成年犬OCE中含有清除自由基、增强抗氧化能力的特殊物质。并且低浓度OCE较高浓度OCE对体外培养的视网膜组织抗氧化作用显著。     

不同条件体外培养的视网膜组织中NO及其合成酶变化

目的 :观察不同成份的培养液对成年犬视网膜组织进行体外培养的前后NO及其合成酶的改变 ,旨在为视网膜移植提供抗氧化能力的保护性方法。方法 :健康成年家犬 3 7只 (74眼 ) ,将动物随机分成六组 ,Ⅰ (新鲜视网膜组 )Ⅱ (常规培养液组 )Ⅲ (高浓度OCE组 )Ⅳ(低浓度OCE组 )Ⅴ (高浓度全脑组织提取液组 )Ⅵ (低浓度全脑组织提取液组 )培养一周。六组视网膜组织匀浆 ,离心 ,取上清液后进行NO、NOS生化指标的测定。结果 :Ⅰ～Ⅵ组视网膜组织NO、NOS含量差异有显著性。与Ⅰ组相比 ,Ⅱ、Ⅲ、Ⅴ、Ⅵ组NO、NOS值显著增高 ;与Ⅱ组相比Ⅲ、Ⅳ组NO、NOS值显著降低 ;且Ⅳ组与Ⅰ组NO值无统计学差异。Ⅳ组与Ⅲ组比较 ,NOS值降低明显。结论 :成年犬OCE中含有清除自由基、增强抗氧化能力的特殊物质。并且低浓度OCE较高浓度OCE对体外培养的视网膜组织抵抗NO的能力显著。     

雌激素对视网膜光损伤的保护作用

目的：探讨雌激素对光诱导的视网膜感光细胞凋亡的抑制作用及其 机制。 方法：雌性Sprague－Dawley （SD）大鼠20只随机分为去势组和去势+雌激素组，每组各10只大鼠。 接受12h亮、12 h暗(12∶12)的循环光照射，光照强度（600.0±35.4） lx，共14次。所有 大鼠摘除 右眼球，测量视网膜外核层的厚度，脱氧核糖核苷酸末端转移酶介导的缺口末端标记（TUNE L）法检测视网膜外核层凋亡的感光细胞，免疫组织化学染色结合图像分析系统观察视网膜 一氧化氮合酶（NOS）的表达及分布。 结果：光照后去势组外核层薄于去 势+雌激素组。去势 组、去势+雌激素组外核层被TUNEL法标记的阳性凋亡细胞数分别为 (0.0275±0.0069)、 (0.0162±0.0054) 个/μm²，两组间差异有统计学意义（t=4.1370，P=0.0012）。去势组及去势+雌激素组视网膜内核层NOS阳性着色细胞的积分吸光度［A，旧称 光密度（OD）］值分别为0.3675±0.0662、0.2941±0.0350，两组间差异有统计学意义（t=3.4885，P =0.0031）。 结论：雌激素可通过调控NOS的合成、抑制感光细胞的凋 亡而对视网膜光损伤起保护作用。     

Eales 病患者视网膜光凝治疗前后血浆一氧化氮及一氧化氮合酶活性的变化

目的观察和分析Eales病患者视网膜光凝治疗前后血浆一氧化氮（NO）及一氧化氮合酶（NOS）活性的变化。方法选取80例（131只眼）Eales病患者作为观察组，将其中接受视网膜光凝治疗的44例患者（60只眼）作为激光治疗组，将其中未接受视网膜光凝治疗的36例患者（71只眼）作为非激光治疗组，选取40例排除眼病的健康人作为对照组。对所有研究对象治疗前及激光治疗组患者术后1、3、6个月的血浆NO水平及血浆总NOS（ tNOS）、结构型NOS（cNOS）和诱导型NOS（iNOS）水平进行检测和比较，并对激光治疗组患者的治疗有效率和视力恢复情况进行评价。结果观察组患者的血浆NO水平、tNOS水平、cNOS水平均显著低于对照组（t ＝6．128、3.465、4．053，P ＜0．05），激光治疗组与非激光治疗组患者治疗前的血浆NO水平、tNOS水平、iNOS水平、cNOS水平的差异均无统计学意义（t ＝0．625、0．511、0．426、0．637，P ＜0．05）；经视网膜光凝治疗后，激光治疗组中视力稳定或提高的患眼数占全部患眼的90％，疗效评价有效的患眼数占全部患眼的88．3％，而患者在治疗前，术后1、3、6个月各时点的血浆NO水平、tNOS水平、iNOS水平、cNOS水平的差异均无统计学意义（F ＝0．728、0．635、0．608、0.942，P ＜0．05）。结论 Eales病患者表现为血浆NO、NOS水平显著下降，但这一变化的程度与其视网膜病变程度无关，视网膜光凝治疗能够有效缓解患者的视网膜病变、恢复患者的视力，但对于纠正上述引发Eales病的病理机制无显著作用。     

脂联素调控糖尿病大鼠视网膜一氧化氮合酶的表达及意义

背景糖尿病视网膜病变（DR）是糖尿病最常见的微血管并发症,其发病机制尚未完全阐明。脂联素可以通过抑制血管内皮细胞的炎症反应、降低血管细胞间黏附能力等影响糖尿病微血管病变的发生,脂联素与一氧化氮合酶（NOS）的作用关系报道较少。目的观察脂联素对糖尿病大鼠视网膜NOS表达的影响。方法选择8～10周龄雌性SD大鼠40只,按随机数字表法将大鼠分为正常对照组10只、脂联素组及糖尿病对照组各15只。脂联素组及糖尿病对照组大鼠用一次性腹腔注射四氧嘧啶法建立糖尿病模型,注射24h后测空腹血糖值〉16mmol／L、尿糖〉＋＋＋为造模成功,纳入研究共24只糖尿病大鼠。脂联素组大鼠给予10μg／kg重组脂联素注射。采用Westernblot法检测脂联素蛋白在正常对照组、脂联素组及糖尿病对照组大鼠视网膜中的定量变化,采用免疫组织化学法观察NOS在各组大鼠视网膜中的表达和定位。结果正常对照组、脂联素组及糖尿病对照组大鼠视网膜中脂联素蛋白含量（脂联素／p—actin）分别为0．85±0．21、0．79±0．17和0．42±0．08,总体比较差异有统计学意义（,=4．236,P=0．000）;糖尿病对照组大鼠视网膜脂联素蛋白较正常对照组和脂联素组明显下降,差异均有统计学意义（q=6．615,P=0．000;q=6．026,P=0．000）。正常对照组、脂联素组、糖尿病对照组NOS阳性反应强度的4值分别为0．244±0．035、0．262±0．032和0．367±0．066,总体差异有统计学意义（F=3．752,P=0．001）;糖尿病对照组NOS含量较正常对照组、脂联素组明显升高,差异均有统计学意义（q=3．488,P=0．002;q=3．079,P=0．005）。NOS主要表达于视网膜内核层和视网膜神经节细胞（RGCs）层。结论脂联素可下调糖尿病大鼠视网膜中NOS的含量,减少NO在视网膜中的生成,减轻NO对视网膜血管内皮细胞结构和功能的损伤,从而延缓DR的发生。     

急性高眼压状态大鼠视网膜一氧化氮 及其合酶变化的研究

目的通过对急性高眼压下大鼠视网膜一氧化氮(nitric oxid e,NO)及其合酶(nitric oxide synthase,NOS)变化的分析,探讨一氧化氮在高眼压视网膜损伤中的作用。方法Wistar大鼠60只,随机分成为高眼压30 min组;高眼压60 min组;高眼压90 min组;高眼压后12 h组和高眼压后24 h 组。前房加压灌注成高眼压模型。利用镀铜镉还原法测定视网膜中NO₂^－/NO₃^－ 的 含量从而间接反映视网膜组织中NO的含量。利用免疫组织化学法研究视网膜内神经结构型一氧化氮合酶(neuronal constitutive nitric oxide synthase,ncNOS)的分布及其变化。结果正常及缺血大鼠视网膜神经结构型一氧化氮合酶(ncNOS)主要位于大鼠视网膜内核层内侧,节细胞层,内丛状层。急性高眼压30min,60min ,90min大鼠视网膜NO的含量逐渐下降(P<0.01),ncNOS阳性 细胞数也逐渐减少(P<0.05),阳性物质表达减弱;急性高眼压 90min后再灌注过程中,NO的含量比90min时明显升高(P<0.05),但与正常比较仍显著下降(P<0.01)。ncNOS阳性细胞数继续减少(P <0.01)。结论一氧化氮参与了急性高 眼压下视网膜损伤过程;通过ncNOS催化的途径合成的NO对缺血以及缺血再灌注的视网膜可能具有重要的作用。(中华眼底病杂志,2001,17:230-233)     

一氧化氮与视网膜微循环

一氧化氮（NO）是体内一氧化氮合酶（NOS）催化L-精氨酸（L-arg)生成的内源性反应气体，它通过升高细胞内环磷酸鸟苷（cGMP)含量而参与眼部生理，病理过程。本主要对一氧化氮调节视网膜微循环作一综述。     

一氧化氮及其合酶与糖尿病视网膜病变发病关系的研究进展

一氧化氮(nitric oxide,NO)是由一氧化氮合酶(nitric oxide synthase,NOS)催化合成的一种重要的信号分子和生物活性物质.目前的研究表明,NO及NOS在糖尿病视网膜病变(diabetic retinopathy,DR)的发生、发展中发挥重要的作用,因此NO及NOS成为当今治疗干预DR的一个研究热点,本文主要就NO及NOS与DR发病关系的研究进展作一综述.     

米诺环素对大鼠视网膜诱导型一氧化氮合酶表达的影响

目的探讨米诺环素对大鼠视神经损伤后的保护作用。方法观察米诺环素对诱导型一氧化氮合酶（iNOS）表达的影响。成年SD大鼠54只（右眼54只）,随机分为正常组6只（右眼6只）、实验组24只（右眼24只）、对照组（右眼24只）。后两组均制备右眼视神经钳夹伤模型,伤后1h分别给予45mg／kg米诺环素和等量生理盐水腹腔注射,此后1次／d。于伤后1、3、7、14d取材,观察视网膜组织形态学变化,利用计算机图像分析技术对经免疫组织化学染色后视网膜组织中iNOS表达的平均光密度值进行半定量检测。结果1d、3d,7d及14d实验组iNOS表达水平明显较对照组降低（t1d=9．497、t3d=11．203、t7d=15．622、t14d=4．889,均P〈0．001）。结论米诺环素可通过抑制视神经钳夹伤后视网膜组织中iNOS的表达,而对损伤视神经起到抗氧化和抗凋亡作用。     

角膜碱烧伤房水一氧化氮及一氧化氮合酶变化

目的探讨角膜碱烧伤后房水一氧化氮（NO）与炎症反应的关系。方法用健康家兔动态观察对照组、实验组和对侧眼组眼内炎症反应及房水一氧化氮合酶（NOS）和NO2^-／NO3^-的活性。结果角膜碱烧伤后炎症反应与房水NOS和NO活性呈动态变化，实验组明显高于对侧眼组，且两组均高于对照组。结论房水NO的变化与角膜碱烧伤后的眼内炎症反应密切相关。     

The levels of cytokines and nitric oxide in rabbit vitreous humor after retinal laser photocoagulation

OBJECTIVE: To determine the levels of nitric oxide (NO) and cytokines such as interleukin 1-beta (IL-1beta), interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha) on vitreous humor following retinal laser photocoagulation. MATERIALS AND METHODS: The rabbits were divided into 3 groups of 4 animals (8 eyes) each. Twelve pigmented rabbit eyes underwent modified grid pattern photocoagulation with a power of 240 mW (group I); 300 mW (group II); and 360 mW (group III). The eyes received 200 burns using a spot size of 200 micro, and duration of 0.2 s. Vitreous humor samples were collected from each eye preoperatively and at 24 and 72 hours after the laser. RESULTS: When compared to preoperative levels, IL-6 levels were increased in all groups; IL-1beta levels were increased significantly only in group III. IL-8 levels were high in groups II and III only at 72 hours (P <0.05). TNFalpha levels were elevated significantly in group II and III only at 24 hours (P <0.05). NO levels were significantly higher than preoperative values in all groups at all times. CONCLUSION: Our results support that especially IL-6, IL-8, and NO levels increase significantly following laser photocoagulation. This preliminary study suggests that IL-6, IL-8, and NO might be dominant contributing factors in the occurrence of the inflammation postoperatively.     

倍他洛尔与氨基胍对大鼠视网膜缺血再灌注损伤的保护作用

目的:通过观察在大鼠急性高眼压模型中视网膜一氧化氮合成酶(nitric oxide synthase,NOS)分布及含量的变化,并检测视网膜丙二醛(malondialdehyde,MDA)水平的变化,探讨氨基胍(aminoguanidine,AG)与倍他洛尔(betaxolol)对大鼠高眼压视网膜缺血再灌注损伤的保护作用。方法:采用前房穿刺加压法建立大鼠缺血再灌注损伤模型,维持灌注时间60min。将各组右眼球经视神经矢状切片标本做HE染色进行视网膜组织学观察,还原型尼克酰胺嘌呤二核苷酸磷酸-黄递酶(NADPH-d)法检测视网膜NOS染色阳性的细胞数,硫代巴比妥酸(thiobarbituric acid,TBA)法测定各组左眼球视网膜MDA含量。结果:各组视网膜均有NOS表达,NOS阳性细胞在视网膜主要分布于视网膜节细胞层(ganglion cell layer,GCL)、内丛状层(inner plexiform layer,IPL)、内核层(inner nuclearlayer,INL),200倍视野计数生理盐水组视网膜GCL的NOS阳性细胞数明显高于空白对照组(P<0.01);AG与betaxolol药物治疗各组的NOS阳性细胞数较生理盐水组减少(P<0.05);视网膜NOS阳性细胞数与视网膜MDA含量增减呈正相关性(r=0.69,P<0.01)。结论:AG通过对诱导型NOS的抑制在大鼠高眼压诱导视网膜损伤中起到视神经保护作用。betaxolol通过抑制钙通道,使NO的生成减少,增加抗氧化能力,从而起神经保护作用。     

Effects of lens extirpation with anterior vitrectomy on vitreous three-dimensional mesh structure

AIM: To investigate the changes in vitreous gel structure after lens extirpation combined with anterior vitrectomy in rabbit eyes. METHODS: Twenty-eight chinchilla rabbits were divided into three groups. The control group (Group I) included 16 eyes from eight rabbits who did not receive any treatment. Group II included 20 eyes from 10 rabbits that underwent lens aspiration only. Group III included 20 eyes from 10 rabbits that underwent lens aspiration combined with posterior capsulotomy and anterior vitrectomy. Eyes were harvested on the 30th and 60th day postoperatively, respectively. Changes in vitreous gel stretch length due to gravity and the rate of vitreous liquefaction were observed. The collagen content in the vitreous body was examined using the L-hydroxyproline test. Electronic microscopic images were obtained from each eyeball. RESULTS: On both the 30th and 60th day postoperatively, the vitreous gel length of group III was significantly shorter than group I and group II (P<0.05), while the rate of liquefaction of the vitreous body in group III was significantly higher than group I and group II (P<0.05). The collagen content in group III was also higher than that in group I and group II (P<0.05). CONCLUSION: Loss of vitreous gel mass is more likely to occur in the eyes of rabbits receiving anterior vitrectomy. Lensectomy combined with anterior vitrectomy may damage the stable three-dimensional mesh structure of collagen, which could aggravate vitreous gel liquefaction.     

神经生长因子联合银杏叶提取物对兔急性青光眼视网膜缺血再灌注损伤的保护作用

目的:探讨神经生长因子联合银杏叶提取物对兔实验性高眼压视网膜缺血再灌注(retinal ischemia reperfusion,RIR)损伤的保护作用.方法:建立兔青光眼缺血再灌注模型,72只新西兰大白兔随机分为神经生长因子组(A组)、银杏叶提取物组(B组)和联合用药组(C组).分别在持续给药1、7、14d,光镜下观察视网膜各层组织形态学改变,测定视网膜组织中超氧化物歧化酶(superoxide dismutase,SOD)、一氧化氮(nitric oxide,NO)、丙二醛(malondialdehyde,MDA)浓度变化.结果:在持续给药1、7、14d,银杏叶提取物组、神经生长因子组的MDA含量和NO含量均高于联合用药组(P<0.05);各时间点,银杏叶提取物组、神经生长子组的SOD含量均低于联合用药组(P<0.05).HE染色视网膜神经节细胞(retinal ganglion cells,RGCs)计数结果显示,联合用药组RGCs的丢失较其他组明显减少,各时间点银杏叶提取物组、神经生长因子组的RGCs计数均低于联合用药组(P<0.05).结论:神经生长因子联合银杏叶提取物对RIR损伤具有更好更持久的保护作用,机制可能与其降低自由基的大量产生,以及其增加视网膜组织中SOD含量和活性有关.     

Localization of nitric oxide synthase isoforms in porcine ocular tissues.

PURPOSE: To determine by immunohistochemistry the distribution of different nitric oxide synthases (NOS) isoforms in the porcine eye. METHODS: By light microscopy (immunofluorescence), porcine ocular tissues were investigated using monoclonal antibodies against neuronal NOS (nNOS; NOS I), endothelial NOS (ecNOS; NOS III), and macrophage NOS (macNOS; NOS II). RESULTS: Specific nNOS immunoreactivity was detected along the apical cytoplasmic portions of the non-pigmented and pigmented ciliary epithelial cells, in the endothelial lining of the corneoscleral meshwork and the uveal cords of the iridocorneal angle tissue, as well as in the photoreceptor layer of the sensory retina. Immunoreactivity for ecNOS was confined to the vascular endothelium of the vessels of the conjunctiva, iris, ciliary body, retina, choroid and optic nerve. A mild immunostaining for macNOS was present in the cytoplasm of some non-pigmented ciliary epithelial cells. CONCLUSIONS: The predominant localization of nNOS in ciliary epithelial and trabecular endothelial cells suggests a possible involvement of nNOS in both the production and outflow of aqueous humor in porcine eyes.     

Preretinal membrane formation in rabbit eyes after intravitreal transplantation of cultured astrocytes

Astrocytes were cultured from the cerebral cortices of newborn rabbits and were so confirmed by staining of the glial fibrillary acidic protein (GFAP). In Experiment I, the astrocytes of newborn rabbits of both sexes from one mother were pooled and suspended in a culture medium, and approximately 1-2 X 10(4) cells were injected into the vitreous cavity of one eye and the culture medium alone was injected into the fellow eye of the mother rabbit. In Experiment II, the astrocytes cultured from the cerebral cortex of a single newborn rabbit of known sex were injected into both eyes of the mother or father rabbit. In the 24 eyes receiving the astrocyte injection, 22 eyes developed preretinal membrane in 2.5 to 14 weeks: 11 eyes developed traction retinal detachment. In the 12 control eyes receiving the culture medium injection, preretinal membrane was seen only in one eye. The preretinal membrane consisted predominantly of spindle-shaped cells positively stained by the peroxidase-antiperoxidase method for GFAP staining. Electron microscopy showed that the major component cells of the preretinal membrane were astrocytes with characteristic intermediate filaments; no retinal pigment epithelial cells were observed. In Experiment II, the average frequency of sex chromatin detection was 4.6% and 55.2% in the male and female astrocyte cultures, respectively. Three groups of experiments were made, A) the female astrocytes injected into the mother's eyes, B) the male astrocytes injected into the mother's eyes and C) the female astrocytes injected into the father's eyes. The sex chromatin was found in the cells of the preretinal membrane at the average frequencies of 63.5%, 34.4% and 55.5% in Groups A, B and C, respectively. It was concluded that the astrocytes injected into the vitreous cavity proliferated and formed the preretinal membrane to a degree that caused traction retinal detachment, without involvement of the retinal pigment epithelial cells. It was also thought that the astrocytes from the retina of the adult host eyes participated to some extent in the preretinal membrane formation.     

羊膜对人视网膜色素上皮细胞增生和分化的影响

背景人视网膜色素上皮（RPE）细胞移植治疗视网膜变性性疾病是目前的研究热点之一,许多生物载体可制备RPE细胞单层,但多存在着细胞毒性、稳定性差及免疫反应等问题。目的检测羊膜对人RPE细胞增生和分化的影响,探讨其作为人RPE细胞层载体进行移植的可能性。方法将RPE细胞系ARPE-19细胞株用含质量分数10％胎牛血清的DMEM／F12培养基进行培养和传代,8～12代细胞用于实验。将传代细胞分为2个组,一组细胞接种于去上皮羊膜作为实验组,另一组细胞直接在培养孔内进行培养作为对照组。分别于接种后24、48、72、96h行MTT实验,测定RPE细胞的吸光度（A492）值以评估两组细胞在增生能力方面的不同;培养3周后的细胞层行苏木精-伊红染色,检测细胞在不同培养载体上是否存在形态学方面的区别;分别收集同一孔中生长于羊膜和培养板表面的细胞,采用逆转录聚合酶链反应（RT—PCR）法检测色素上皮衍生因子（PEDF）、钙黏蛋白（N—cadherin）、β-连环蛋白（β—catenin）以及细胞连接相关蛋白的表达情况;同时收集培养3周时的细胞行透射电子显微镜和扫描电子显微镜检查,比较不同载体培养的ARPE-19细胞在超微结构方面的区别。结果与对照组相比,实验组细胞增生的速度明显变缓,两组细胞增生情况比较差异有统计学意义（F=41．760,P=0．000）。苏木精-伊红染色结果显示,同一培养孔内实验组的细胞密度明显低于对照组,说明羊膜对ARPE-19细胞增生的影响不是通过细胞分泌的可溶性因子的作用。RT—PCR结果显示,实验组细胞连接相关蛋白claudin 1、N—cadherin和PEDF mRNA在培养细胞上的表达水平均明显高于对照组,差异均有统计学意义（t=15．828,P=0．000;t=6．839,P=0．002;t=14．667,P=0．000）;Connexin 43的表达低于对照组,差异有统计学意义（t=3．358,P=0．024）。超微结构分析发现羊膜载体上的细胞呈典型的多边形RPE细胞表型,分化现象明显,而普通培养板培养的RPE细胞形态主要呈梭形,细胞层厚薄不均。结论去上皮羊膜为载体培养的RPE细胞增生速度变慢,但培养的细胞分化程度较高,提示羊膜可作为RPE细胞体外培养的良好载体,用于制备移植所需功能成熟的RPE细胞片层。     

复方卡波姆诱发的兔高眼压模型与其它兔高眼压模型的比较研究

目的 建立适用于研究抗青光眼药物降眼压作用及保护视神经作用的兔青光眼模型。方法 将21只兔随机分为I、Ⅱ、Ⅲ及Ⅳ组,分别对其前房内注射复方卡波姆、甲基纤维素及复方甲基纤维素,结膜下注射地塞米松诱发青光眼,并对4种药物诱发的青光眼模型进行观察。结果 I组高眼压持续20－50d,平均眼压为29－35mmHg(1mmHg=0.133kPa),眼压峰值为37－45mmHg,青光眼模型成功率为91．7％。Ⅱ及Ⅲ级模型有10－20％的兔眼眼压升主持续3－4d,如按眼压为22mmHg持续1周的标准判断,Ⅱ及Ⅲ组模型均不理想。Ⅳ组眼压平均升高3mmHg,持续7d,亦为失败模型。结论 复方卡波姆诱发的兔青光眼模型具有引起眼压中度、稳定升高的时间长,方法简单,易于操作和控制等优点。可用于对青光眼性视神经视网膜损害的研究及对抗青光眼药物的研究,是一种较理想的兔青光眼模型。     

Notch-1调控视网膜前体细胞向视网膜神经节细胞分化

目的研究Notch-1对视网膜前体细胞(RPC)向视网膜神经节细胞(RGC)分化的调控作用。方法分离培养胚胎14 d龄Sprague-Dawley大鼠的RPC，实验组和对照组分别用含有Notch-1反义寡核苷酸链和无关序列寡核苷酸链的培养液进行诱导分化14 d，倒置相差显微镜每天观察细胞的生长和分化情况，Thy1.1标记RGC并进行计数。结果实验组和对照组的RPC都能分化为多种视网膜细胞类型，包括Thy1.1阳性的RGC，但两组RPC向RGC分化的百分比不同。实验组和对照组RGC的百分比分别为(16.57±4.31)%和(31.19±6.90)%，两组比较差异有统计学意义（t=9.84,P＜0.001）。结论Notch-1对RPC的分化具有负向调控作用，阻断Notch-1能促进RPC向RGC分化。(中华眼底病杂志, 2007, 23: 101-103)