5-羟色胺在豚鼠离焦性近视眼中含量的变化

目的:探讨5-羟色胺(5-hydroxytryptamine,5-HT)在豚鼠近视离焦模型形成中的作用。方法:将24只4周龄的豚鼠分成2组,离焦组(18只36眼),包括离焦实验眼(右眼,戴接触镜)和离焦对照眼(左眼,未戴接触镜);空白对照组(6只12眼)除检查外不做任何干预。将PMMA接触镜配戴在离焦组豚鼠右眼前,自然光下饲养14d后除去镜片,建立近视离焦模型。近视离焦模型建立后,分别处死实验组及空白对照组豚鼠,取出眼球,分离出视网膜、脉络膜及巩膜组织。用高效液像色谱电化学检测法测定视网膜、脉络膜及巩膜组织中5-HT含量。结果:在豚鼠视网膜、脉络膜、巩膜内均有5-HT存在,其中脉络膜中含量最高,其次为巩膜及视网膜;离焦实验眼视网膜、脉络膜及巩膜中5-HT含量明显升高(P<0.01);与离焦对照眼及空白对照组相比较差异显著(P<0.05)。结论:5-HT可能参与了离焦性近视的形成。     

胞内视黄醛结合蛋白在豚鼠离焦诱导型近视眼中的表达

目的探讨胞内视黄醛结合蛋白（CRALBP）在豚鼠离焦诱导型近视眼中的表达。方法选取3～4周龄有色豚鼠10只,右眼戴-8．00D透镜,左眼不戴镜作为对照眼。戴镜前和戴镜后第11d分别测量眼轴长度和屈光度;通过免疫组织化学和蛋白质免疫印迹的方法检测CRALBP在豚鼠诱导近视眼和对照眼的视网膜、脉络膜和巩膜中的表达。结果戴镜后第11d,模型眼与戴镜前相比屈光度平均增加了一3．17D,与对照眼比较差异有统计学意义（P〈0．01）;眼轴长度在两组眼之间差异无统计学意义（P〉0．05）。免疫组织化学结果显示,与对照眼相比,诱导近视眼的CRALBP在巩膜中的表达明显降低,在脉络膜和视网膜中的表达升高。Westernblot结果和免疫组织化学结果一致,CRALBP在诱导近视眼巩膜中的表达明显降低。结论CRALBP可能在豚鼠诱导近视眼的发生以及巩膜重塑中起一定作用。     

电针对透镜诱导性近视豚鼠闪光视网膜电图的影响

目的　探讨电针对透镜诱导性近视豚鼠闪光视网膜电图（ｅｌｅｃｔｒｏｒｅｔｉｎｏｇｒａｍ,ＥＲＧ）的影响。方法　２４只３周龄健康三色短毛豚鼠随机分为透镜诱导组（１２只）与透镜诱导＋电针组（１２只）。两组豚鼠右眼戴－１０Ｄ透镜,左眼不戴镜作为自身对照。透镜诱导＋电针组在戴镜的同时,电针刺激豚鼠两侧合谷穴与太阳穴。４周后测量２组屈光度、眼轴长度及ＥＲＧ波形的变化。结果　４周后,与自身对照眼比较,透镜诱导眼近视屈光度增加（Ｐ＜０．０１）,眼轴延长（Ｐ＜０．０１）;同时其暗适应振荡电位的ＯＳ２波振幅及总振幅下降（均为Ｐ＜０．０１）,暗适应最大混合反应、明适应视锥细胞反应的ｂ波振幅下降（均为Ｐ＜０.０１）。电针干预后,透镜诱导眼的屈光度和眼轴长度没有变化（Ｐ＞０．０５）;但与透镜诱导组右眼相比,透镜诱导＋电针组透镜诱导眼暗适应振荡电位的ＯＳ２波振幅及总振幅,暗适应最大混合反应、明适应视锥细胞反应的ｂ波振幅均增高（均为Ｐ＜０．０５）,达到与其自身对照眼相似的水平（均为Ｐ＞０．０５）。结论　电针刺激合谷穴与太阳穴影响透镜诱导性近视豚鼠ＥＲＧ,可使其恢复至正常水平。     

豚鼠形觉剥夺性近视眼视网膜、脉络膜多巴胺代谢的变化

目的研究形觉剥夺对豚鼠神经视网膜、视网膜色素上皮（retinal pigment epithelium,RPE）／脉络膜复合体多巴胺（dopamine,DA）代谢的影响。方法28日龄豚鼠36只,分为3组：正常对照组、遮盖组、遮盖＋去遮盖组,每组12只。遮盖组用半透明眼罩遮盖豚鼠右眼14d,遮盖＋去遮盖纽在遮盖11d后去遮盖3d。14d后测定角膜曲率半径、眼球屈光度和眼轴长度。处死豚鼠,取眼后极部视网膜、脉络膜组织,用免疫组化染色和Western blotting法检测酪氨酸羟化酶（tyrosine hydroxylase,TH）蛋白在神经视网膜、RPE／脉络膜复合体的表达情况,用高效液相色谱检测神经视网膜、RPE／脉络膜复合体的DA、二羟基苯乙酸（3,4-dihydroxyphenylacetic acid,DOPAC）的含量。结果TH蛋白阳性表达于视网膜神经节细胞和内核层部分细胞,RPE／脉络膜复合体中表达阴性。遮盖14d后,豚鼠遮盖眼眼轴延长,近视形成,神经视网膜TH蛋白表达量和DA、DOPAC含量降低（P〈0．05）。遮盖＋去遮盖纽的遮盖眼近视程度低于遮盖组．其神经视网膜TH蛋白表达量和DA、DOPAC含量升高（P〈O．05）,但仍低于正常对照组（P〈O．05）。各纽豚鼠RPE／脉络膜复合体的DA、DOPAC含量比较,差异无统计学意义（P〉0．05）。结论形觉剥夺能调控豚鼠神经视网膜DA代谢,但不影响RPE／脉络膜复合体的DA代谢。     

电针对负透镜诱导型近视豚鼠视网膜M1受体表达的影响

目的　探讨电针对负透镜诱导型近视豚鼠视网膜中毒蕈碱样乙酰胆碱Ｍ１受体表达的影响。方法　４８只３周龄豚鼠随机分为４组:正常对照组、近视模型组、近视电针组与近视假穴组,后３组豚鼠右眼配戴－１０．００Ｄ透镜片,建立透镜诱导型近视豚鼠动物模型,近视电针组戴镜同时给予针刺豚鼠的合谷穴和太阳穴,近视假穴组针刺臀部无穴位处。于造模前及造模后４周测量各组眼轴长度和屈光度,同时取视网膜组织,利用ＲＴ-ＰＣＲ的方法检测各组豚鼠视网膜中Ｍ１受体ｍＲＮＡ的相对表达量,ＥＬＩＳＡ法检测Ｍ１受体的蛋白含量。结果　造模４周后,近视模型组右眼屈光度为（－３．４０±０．５５）Ｄ,明显低于正常对照组右眼的（１．２０±０．２４）Ｄ和自身对照眼左眼的屈光度（１．２５±０．３２）Ｄ（均为Ｐ＜０．０５）;近视模型组右眼眼轴长度为（８．７４±０．３８）ｍｍ,明显大于正常对照组的右眼眼轴长度（８．２３±０．２１）ｍｍ,也大于自身对照眼左眼的眼轴长度（８．１６±０．４３）ｍｍ（均为Ｐ＜０．０５）;近视模型组、近视电针组和近视假穴组右眼的眼轴长度和屈光度比较差异均无统计学意义（均为Ｐ＞０．０５）。正常对照组、近视模型组、近视电针组、近视假穴组视网膜中Ｍ１受体的ｍＲＮＡ相对表达量分别为５９．１７±４．０２、７４．５０±４．６４、６４．８３±６．０５和７４．６７±３．９３,Ｍ１受体蛋白含量分别为（９８４．６７±４４．６９）ｎｇ·Ｌ－１、（１１７２．００±４１．９１）ｎｇ·Ｌ－１、（１０２７．００±４１．０８）ｎｇ·Ｌ－１和（１１５３．５０±５６．４０）ｎｇ·Ｌ－１,统计学分析显示正常对照组与近视电针组相比差异无统计学意义（Ｐ＞０．０５）,两组分别与近视模型组和近视假穴组相比差异均有统计学意义（均为Ｐ＜０．０５）。结论　负透镜诱导型近视豚鼠视网膜中Ｍ１受体表达增高,针刺合谷穴和太阳穴可以减少其视网膜中Ｍ１受体表达,这可能是针刺改善近视患者远视力的机制之一。     

全反视黄酸在豚鼠近视形成中的作用

目的探讨全反视黄酸在豚鼠近视形成中的作用。方法选取4周龄英国短毛豚鼠48只,用0.25%托吡卡胺每5 min散瞳3次,45 min后以带状光检影法测定其屈光不正状态。用康宁动物A超仪(KM-1800)测定玻璃体腔深度和眼轴长。实验组24只随机选取一眼于暗光下球旁注射0.4 g/L浓度全反视黄酸0.2 ml,4周后以同样方法检测豚鼠屈光不正状态、玻璃体腔深度和眼轴长,并取眼球做病理学检查。结果实验组处理前眼屈光不正值为(3.73±0.75)D,玻璃体腔深度为(3.09±0.67)mm,眼轴长为(6.44±0.27)mm;对照组眼屈光不正值为(3.72±0.83)D,玻璃体腔深度为(3.19±0.74)mm,眼轴长为(6.54±0.38)mm,实验组和对照组三项参数比较差异均无显著性(P分别为0.96,0.68及0.26)。4周后对照组屈光不正值为(3.56±0.80)D,玻璃体腔深度为(3.57±0.54)mm,眼轴长为(7.80±0.26)mm,实验处理眼屈光不正值为(0.90±1.25)D,玻璃体腔深度为(3.98±0.68)mm,眼轴长为(8.50±0.39)mm。实验组和对照组三项参数间比较差异有非常显著性(三者均P<0.001)。病理检查提示,实验眼较对照眼相同部位的脉络膜变薄,脉络膜中的黑素细胞增加,色素上皮层粗糙,外丛状层增厚,巩膜层厚度增加。结论局部的全反视黄酸应用可诱导豚鼠近视漂移,提示它是动物模型中近视的信使。它可能首先通过使脉络膜变薄引起玻璃体腔的深度增加,从而致视网膜成像焦点落后导致近视。但增多的视黄酸是近视的起始信使还是近视过程中的产物尚需进一步的研究。     

Comparison of form-deprived myopia and lens-induced myopia in guinea pigs

AIM: To study the efficacy difference between form-deprived myopia (FDM) and lens-induced myopia (LIM), the degree of myopia, axial length and pathological changes of the posterior sclera from guinea pigs were evaluated.METHODS: Four-week pigmented guinea pigs were randomly assigned into 3 groups, including normal control (n=6), FDM group with monocular cover (n=11) and LIM group with monocular -7D lens treatment (n=11). FDM group was form-deprived while LIM group was lens-induced for 14 d. Refractive error and axial length were measured prior to and post treatment, respectively. Morphological changes of sclera were examined using both light and electronic microscopes.RESULTS: After 14d treatment, refractive errors for FDM group and LIM group were -3.05±0.71D and -2.12±1.29D, respectively, which were significantly more myopic than that of normal controls and fellow control eyes (P<0.01). As for axial length, it was 7.93±0.03 mm for FDM group and 7.89±0.06 mm for LIM group, which were significantly longer than both normal and fellow controls (P<0.01). With respect to both refractory error and axial length, the differences between FDM group and LIM group were not significant (P>0.05). Under light microscope, both FDM group and LIM group showed thinned sclera, disarrangement of fibrosis and enlarged disassociation between fibers. Consistently, ultrastructural examination showed degenerated fibroblasts and thinned fibers in posterior sclera.CONCLUSION:Following two weeks of myopia induction in guinea pigs, with regard to the degree of myopia, axial length and pathological alterations, there was no significant difference between FDM and LIM models. Therefore, FDM and LIM are equally effective and useful as a model of experimental myopia and guinea pigs are ideal animals for induction of experimental myopia because their high sensitivity to both form-deprivation and lens-induction.     

豚鼠形觉剥夺性近视视网膜中视黄酸转运系统的研究

目的了解视黄醇（RA）转运系统在豚鼠近视发生发展中的作用。方法2周龄英国短毛豚鼠48只,随机分为形觉剥夺组（n=24）和正常对照组（n=24）。形觉剥夺组随机取1只眼,用白色半透明眼罩遮盖形成形觉剥夺,遮盖时间为2周,干预前后均采用睫状肌麻痹后带状光检影法测定其屈光不正状态,用CinescanA/B型超声仪测定玻璃体腔深度和眼轴长度。处死后取视网膜,用HPLC法测定视网膜中的RA水平,Westernblot法定量检测视网膜中视黄酸结合蛋白-Ⅰ（CRABP-Ⅰ）和视黄酸核受体-β（RAR-β）的蛋白水平,并用Real-timePCR法测定其mRNA水平。结果形觉剥夺后模型眼的等效球镜为（-3.82±0.13）D,对照眼为（1.99±0.58）D,差异有统计学意义（t=8.376,P〈0.01）;形觉剥夺组眼轴长度为（8.346±0.047）mm,对照组眼轴长度为（7.888±0.042）mm,差异有统计学意义（t=3.343,P〈0.05）。形觉剥夺组视网膜RA水平较对照组高,差异有统计学意义（t=4.934,P〈0.01）;模型眼视网膜中CRABP-Ⅰ和RAR-β的含量较对照组均提高（P〈0.05）。结论豚鼠形觉剥夺性近视眼视网膜中RA转运系统水平显著上升,RA可能是近视发展的信使。     

Short Wavelength (Blue) Light Is Protective for Lens-Induced Myopia in Guinea Pigs Potentially Through a Retinoic Acid–Related Mechanism

PurposeTo investigate the effect of short-wavelength light (SL) on guinea pigs with lens-induced myopia (LIM) and the possible retinoic acid (RA)–related mechanisms.MethodsTwo-week-old guinea pigs (n = 60) with monocular −5D lenses were reared under white light (WL, 580 lux) or SL (440 nm, 500 lux). The left eyes were uncovered as control. Refractive error (RE) and axial length (AL) were measured at baseline, one week, two weeks, and four weeks after intervention. Retinal RA was measured from four guinea pigs after two and four weeks of treatment with HPLC. Two-week-old guinea pigs (n = 52) with monocular −5D lens were fed with either RA or its synthesis inhibitor citral every third day in the morning, and half from each group were reared under WL or SL conditions. RE and AL were recorded at baseline and two and four weeks after intervention. Retinal RA was measured after four weeks of intervention.ResultsAt the end of treatment, guinea pigs exposed to SL were less myopic than to WL (2.06 ± 1.69D vs. −1.00 ± 1.88D), accompanied with shorter AL (P = 0.01) and less retinal RA (P = 0.02). SL reduced retinal RA even after exogenous RA supplementation (P = 0.02) and decelerated LIM compared to WL (1.66 ± 1.03D vs. −3.53 ± 0.90D). Citral slowed ocular growth, leading to similar RE in W+CI and S+CI groups (3.39 ± 1.65D vs. 5.25 ± 0.80D).ConclusionsOverall, SL reduced LIM in guinea pigs, even in those supplemented with oral RA, accompanied by reduced retinal RA levels. Oral RA accelerated eye elongation, but citral equally decelerated eye elongation under SL and WL with no significant retinal RA reduction.     

外源性视黄酸诱导的豚鼠近视模型的建立

目的建立豚鼠外源性视黄酸诱导近视模型,观察外源性视黄酸在三色豚鼠眼轴生长和屈光变化中的作用。方法选取体质量100g左右3～4d三色豚鼠20只,随机分为正常对照组和视黄酸诱导组。视黄酸诱导组予连续5d喂饲24mg.kg-1花生油调配的视黄酸0.5mL,正常对照组喂饲0.5mL花生油,喂饲前和喂饲后第5天分别测量其眼轴长度、屈光度,观察其变化。用HE染色测量视黄酸诱导组豚鼠巩膜和正常对照组豚鼠巩膜的厚度变化并通过透射电镜观察巩膜成纤维细胞的变化及胶原纤维的改变。结果实验前豚鼠的屈光状态和眼轴长度,两组之间差异均无统计学意义(均为P>0.05)。实验第5天,视黄酸诱导组豚鼠眼轴增长,正常对照组豚鼠的眼轴长度为(7.628±0.009)mm,视黄酸诱导组豚鼠眼轴长度为(7.743±0.005)mm,两组比较差异具有统计学意义(P<0.01);正常对照组的豚鼠眼的屈光度为(+6.50±1.60)D,视黄酸诱导组的豚鼠眼的屈光度(+1.73±0.80)D。与正常对照组相比,视黄酸诱导组的豚鼠眼屈光度平均增加了-4.80D,屈光度差异有统计学意义(P<0.01)。后极部巩膜HE染色显示,视黄酸诱导组巩膜比对照组巩膜薄。透射电镜结果显示,视黄酸诱导组巩膜胶原纤维数量减少,直径变小。结论外源性视黄酸能稳定有效地诱导眼轴增长,形成相对性的近视漂移并直接引起巩膜重塑。     

5-hydroxytryptamine level and 5-HT2A receptor mRNA expression in the guinea pigs eyes with spectacle lens-induced myopia

AIM: To investigate 5-hydroxytryptamine (5-HT) function and 5-HT receptor 2A (5-HT2A) mRNA expression in the formation of lens-induced myopia (LIM). METHODS: Lens-induced myopia construction method was applied to generate myopia on guinea pig right eye (LIM eye). RESULTS: LIM eyes formed significant myopia with longer axial length. 5-HT level in retina, choroids and sclera from LIM eyes was significantly higher than that in control group. 5-HT2A mRNA expression was also significantly up-regulated. CONCLUSION: Refraction lens could induce myopia in guinea pig and 5-HT may play an important role in the formation of myopia by binding with 5-HT2A receptor.     

视黄醛在实验性近视中的作用

近视是一种发育性疾病，近视眼球巩膜的主动扩张是其伸长的重要机制，而视黄醛是眼球发育中重要的信号转导分子，其在脊椎动物的眼球发育中具有多种不同的重要作用。视黄醛可能是调节实验性近视眼球伸长的信使分子近年来有关视黄醛与实验性近视发生，发展的关系的研究取得一定进展，本研究综述了视黄醛及其核受体，实验性近视眼球的视网膜，脉络膜，巩膜的视黄醛改变以及视黄醛作为传递从视网膜到巩膜的眼球伸长信号的信使分子的研究进展情况。     

MFN1在透镜诱导豚鼠近视模型视网膜上的表达及其意义

目的 建立豚鼠光学离焦近视动物模型,初步探索线粒体融合蛋白1(mitochondrial fusion protein 1,MFN1)在光学离焦豚鼠近视动物模型视网膜上的表达.方法 给15只4周龄幼年豚鼠单眼配戴-7.00 D凹透镜,制作光学离焦性豚鼠近视模型,戴透镜眼作为实验眼,另一眼为自身对照眼.戴镜前及戴镜后1周、2周、3周分别进行检影验光和眼轴长度检查,同时于各时间点分别随机处死5只豚鼠,采用免疫组织化学染色检测视网膜中MFN1的表达,双眼眼球参数检查结果比较采用t检验,对免疫组织化学检查结果做描述定性分析.结果 屈光度:豚鼠戴镜前屈光状态均为远视状态,实验眼和对照眼屈光度差异无统计学意义(P＞0.05);用-7.00 D凹透镜经1周、2周、3周光学离焦可以造成豚鼠远视屈光度数逐渐下降,戴镜后1周两组比较差异无统计学意义(p=0.380);戴镜后2周及3周实验眼与对照眼比较,差异均有统计学意义(均为P＜0.01).眼轴长度:戴镜前豚鼠双眼眼轴长度比较,差异无统计学意义(P＞0.05);戴镜后1周、2周、3周对照眼和实验眼的眼轴均较戴镜前明显延长,实验眼与对照眼的眼轴长度比较差异均有统计学意义(均为P＜0.05).免疫组织化学检测结果:双眼视网膜均可见部分视网膜神经节细胞胞浆及胞膜呈黄色或棕黄色着色,但实验眼免疫阳性细胞着色较深,阳性细胞数相对较多;早期豚鼠近视动物模型视网膜上MFN1阳性表达主要见于视网膜神经节细胞,随着透镜诱导时间的延长,MFN1在视锥视杆细胞中也出现袁达,而对照眼无此现象.结论 采用-7.00 D凹透镜能成功诱导光学离焦豚鼠近视动物模型,豚鼠视网膜上可见MFN1表达,随着透镜诱导时间的延长,表达强度和部位逐渐发生变化,提示MFN1可能在近视的发生发展过程中起着一定的作用.     

N-甲基-D-天冬氨酸受体1在形觉剥夺性近视豚鼠视网膜上的表达

目的对豚鼠行形觉剥夺建立近视动物模型，观察离子型谷氨酸受体N-甲基-D-天冬氨酸受体1（N—methyl—D—aspartate receptor 1．NMDAR1）在近视豚鼠视网膜上的动态表达．探讨其在近视发病机制中的作用。方法60只三色豚鼠随机分为3组：未遮盖组（Ⅰ）、单眼遮盖2周组（Ⅱ）、单眼遮盖3周组（Ⅲ），其中右眼遮盖为实验眼，左眼为自身对照眼。对各组进行视网膜检影和A超测眼轴。分别运用免疫组化及Western Blotting法检测各组豚鼠视网膜NMDAR1蛋白表达。结果Ⅰ组双眼呈轻度远视状态．双眼眼轴差异无显著性（P〉0．05）；Ⅱ组实验眼呈轻度近视（-1.583±1.478）D，自身对照眼呈轻度远视（2.500±1.017）D：实验眼眼轴较自身对照眼轻度延长（P〈0．05）；Ⅲ组实验眼呈中度近视（-3．417±l.169）D，自身对照眼呈轻度远视（1.813±1．072）D；实验眼眼轴较自身对照眼明显延长（P〈0．05）。免疫组化显示NMDAR1主要表达在豚鼠视网膜的内核层细胞及神经节细胞。Ⅰ组实验眼视网膜上NMDAR1蛋白含量为0．338±0．314．Ⅱ组实验眼NMDAB1蛋白含量升高为0．464±0．280．Ⅲ组实验眼视网膜NMDAR1蛋白含量明显上调为0．635±0．037;实验眼视网膜上NMDAR1蛋白含量随遮盖时间延长明显上调．与自身对照眼比较差异有显著性（P〈0．05）。结论形觉剥夺可明显上调豚鼠视网膜NMDAR1的蛋白表达，形觉剥夺产生的异常视觉信号可能通过刺激谷氨酸的释放、NMDAR1过度生成，参与近视的调控。     

电针干预对透镜诱导型近视豚鼠视网膜和视皮层中BDNF、NGF及AchE表达的影响

目的 探讨电针干预对透镜诱导型近视(LIM)豚鼠视网膜和视皮层中脑源性神经营养因子(BDNF)、神经生长因子(NGF)及乙酰胆碱酯酶(AchE)表达变化的影响.方法 将90只2周龄雄性豚鼠随机分为正常对照(NC)组、LIM组和LIM+电针治疗(LIM+EA)组.NC组豚鼠正常饲养,不进行干预;LIM组和LIM+EA组豚...     

透镜诱导条件下混合性近视和真性近视豚鼠屈光度和眼轴长度变化

目的 探讨-6.0 D透镜诱导条件下混合性近视和真性近视豚鼠屈光度和眼轴长度变化.方法 选取2周龄睫状肌麻痹前和麻痹后屈光度均在1.00～3.00 D之间的健康英国三色短毛豚鼠20只.将20只豚鼠适应性饲养3 d后,右眼配戴-6.0 D透镜,进行近视模型构建.依据透镜诱导2周后豚鼠睫状肌麻痹前后屈光度差值≥0.5 D且...     

Contralateral effect in progression and recovery of lens-induced myopia in mice

Purpose

Apart from genetic factors, recent animal studies on myopia have focused on localised mechanisms. In this study, we aimed to examine the contralateral effects of monocular experimental myopia and recovery, which cannot be explained by a mere local mechanism.

Methods

One eye of 3-week-old C57BL/6 male mice was fitted with a −30 dioptre (D) lens. The mice were distributed into two groups based on different conditions in the contralateral eye: either no lens (NLC) (n = 10) or a Plano lens on the contralateral eye (PLC) group (n = 6). Mice receiving no treatment on either eye were set as a control group (n = 6). Lenses were removed after 3 weeks of myopia induction. All mice were allowed to recover for 1 week in the same environment. Refractive status, axial length (AL) and choroidal thickness were measured before myopia induction, after 1 and 3 weeks of lens wear and after 1 week of recovery.

Results

One week after removing the lenses, complete recovery was observed in the eyes that wore the −30 D lenses. In both the PLC and NLC groups, the refractive status showed a myopic shift after lens removal. Additionally, the choroid was significantly thinned in these eyes. The −30 D wearing eye showed a significant increase in AL after 3 weeks of lens wear. While the AL of the −30 D wearing eye ceased to grow after the lens was removed, the AL in the PLC and NLC contralateral eyes increased, and the binocular ALs gradually converged.

Conclusions

Recovery of lens-induced myopia was observed in mouse models. In the fellow eyes, the effects, including thinning of the choroid and changes in refractive status, were triggered by contralateral visual cues.     

视黄酸对体外培养豚鼠巩膜成纤维细胞的影响

目的　探讨豚鼠巩膜成纤维细胞体外培养的方法 ,研究视黄酸 (retinoicacid ,RA)对体外培养豚鼠巩膜成纤维细胞(Guineapigscleralfibroblasts ,GSF)增生的影响 ,以期探索近视的发病机制和眼外伤并发症等与纤维增生有关眼病治疗的新途径。方法　豚鼠巩膜成纤维细胞原代培养 ,在 3 -6代GSF在细胞生长的各个时期加入不同浓度的RA ,用流式细胞术 (flowcy tometryFCM)测定细胞周期 ,计算出GSF不同生长时期在不同RA浓度培养时的增生率。结果　在细胞生长的各个时期中GSF的增生率随RA浓度的增加而降低 (P <0 .0 5 )。结论　RA对GSF的增生有明显抑制作用。     

豚鼠形觉剥夺性近视视网膜形态学研究

目的:建立豚鼠形觉剥夺性近视动物模型,研究在豚鼠形觉剥夺性近视眼中视网膜组织病理学改变,探讨其发病机制。方法:出生3wk的三色豚鼠随机分为3组:未遮盖组、单眼遮盖2wk组、单眼遮盖3wk组。对各组进行视网膜检影和A超测眼轴,眼底视网膜光镜及电镜检查以及视网膜各层厚度分析。结果:豚鼠形觉剥夺后近视形成,眼轴延长;视网膜各层变薄,光镜及电镜下均有病理性改变。结论:对豚鼠进行无创性眼罩遮盖可建立有效的形觉剥夺性近视模型。视网膜内层在近视发病机制中起重要作用。     

YS310对豚鼠形觉剥夺性近视作用的实验研究

目的探讨氮氧化酶抑制剂YS310对豚鼠形觉剥夺性近视的治疗作用。设计实验性研究。研究对象豚鼠。方法3￣4周龄三色豚鼠45只,右眼不透明眼罩遮盖,左眼不遮盖,随机分为5组(每组9只):阳性对照组滴用0.1%阿托品,低、中、高浓度用药组分别滴用0.03%、0.1%、0.3%的YS310滴眼液,阴性对照组滴用YS310溶媒,均为右眼给药,每日3次,连续4周。实验前后分别用检影镜和A型超声波测眼屈光度数及眼轴长度。主要指标屈光度数、眼轴长度。结果遮盖4周后,在屈光度数方面,阴性对照组增加了-6.33D。其余各组与阴性对照组相比,阿托品组(增加-4.13D)差异有显著性意义(P=0.011);低浓度组(增加-4.97D)差异无显著性(P=0.066);中浓度组(增加-4.81D)、高浓度组(增加-4.53D)差异有显著性(P=0.041、0.017)。在眼轴方面,阴性对照组增加了0.30mm,阿托品组及低、中、高浓度用药组分别增加了0.22mm、0.29mm、0.27mm、0.26mm,与阴性对照组相比均无显著性差别(P均>0.05)。结论0.1%￣0.3%YS310对豚鼠形觉剥夺性近视的屈光改变有一定的抑制效果,但不能有效地抑制眼轴的增长。(眼科,2006,15:195-197)