豚鼠短期形觉剥夺性近视屈光度眼轴及巩膜改变

目的:观察豚鼠短期形觉剥夺性近视(form deprivationmyopia,FDM)眼轴、屈光度变化及后极部巩膜病理性改变。方法:4周龄健康豚鼠40只,随机分成形觉剥夺实验组和年龄匹配正常对照组各20只。形觉剥夺实验组分为剥夺1,4,7和14d4个亚组,右眼为剥夺眼,采用半透明眼罩遮盖诱导轴性近视,左眼不予处理。对剥夺前后实验组和对照组双眼屈光度、眼轴进行测量,并对后极部巩膜进行HE染色光镜观察和透射电镜观察。结果:形觉剥夺7d近视程度和眼轴长度改变迅速,之后减慢并趋于平稳。4个实验亚组剥夺眼与实验前比较相对近视-0.30±0.45D,-3.65±0.78D,-6.98±0.65D,-8.68±1.12D,相对眼轴延长4.8±3.2,129.0±12.6,159.0±10.1,184.4±10.4μm。其中4,7,14d实验亚组剥夺眼与对照眼差别有统计学差异(P<0.01),剥夺眼后极部巩膜明显变薄,成纤维细胞密度降低,细胞外基质增多。1,4,7,14d实验亚组形觉剥夺眼后极部巩膜胶原纤维平均直径102.0,67.4,52.2,49.8nm,与正常对照眼比较差别有统计学意义(P<0.05)。结论:4周龄豚鼠单眼形觉剥夺4d即可出现轴性近视,1d即有巩膜病理改变,形态学改变先于生物学改变,形觉剥夺7d为近视发展高峰期。     

豚鼠形觉剥夺早期后极部巩膜基质金属蛋白酶2及其抑制剂动态表达

目的探讨豚鼠形觉剥夺性近视（form-deprivation myopia, FDM ）早期后极部巩膜基质金属蛋白酶2（matrix metalloproteinase-2, MMP-2）及基质金属蛋白酶抑制剂2（tissue inhibitor of matrix metalloproteinase-2,TIMP-2）mRNA的表达。方法4周龄三色豚鼠50只,随机分成实验组和正常对照组各25只,实验组又随机分为5组,单眼形觉剥夺（monocular deprivation, MD）右眼1、4、7、14、21d制备FDM动物模型,未遮盖眼为自身对照组。各组豚鼠进行检影验光和A超测量眼轴长度。提取后极部巩膜总RNA,二步法逆转录聚合酶链反应检测各组后极部巩膜MMP-2及TIMP-2mRNA的表达水平。结果除1d外,各组MD后极部巩膜MMP-2mRNA的表达与正常对照组、自身对照组差异均有统计学意义（P〈0,05）,MD组间差异也有统计学意义（P〈0．01）;而TIMP-2mRNA的表达则逐渐下降。各自身对照组MMP-2、TIMP-2mRNA的表达与MD组变化趋势大致相同。结论MMP-2／TIMP-2之间动态平衡失调可能是启动豚鼠FDM巩膜细胞外基质早期主动重塑的重要因素。（中国跟耳鼻喉科杂志,2010,10：75—78）     

RARβ在豚鼠形觉剥夺性近视眼中的表达

目的检测视黄酸受体β（RARβ）在视网膜、脉络膜和巩膜中的表达，探讨RARβ和视黄酸（RA）对哺乳类动物形觉剥夺性近视的作用。方法采用形觉剥夺的方法建立豚鼠眼近视模型。选用1～3d龄健康三色豚鼠45只，随机分为3组，Ⅰ组为持续遮盖8周组，Ⅱ组为遮盖7周后去遮盖1周组，Ⅲ组为遮盖1周组。右眼为遮盖眼，左眼为开放对照眼。测量双眼实验前后的屈光状态及眼轴。应用免疫组织化学和RT-PCR技术检测RARβ的蛋白和mRNA表达水平。结果Ⅰ组诱导出了豚鼠明显的近视改变（P〈0．05）。Ⅱ组去遮盖眼近视度明显降低，眼轴较Ⅰ组短（P〈0．05）。Ⅲ组遮盖眼屈光度和眼轴与对照眼相比差异无显著统计学意义（P〉0．05）。Ⅰ组和Ⅲ组遮盖眼视网膜内核层RARβ蛋白表达高于对照眼（P〈0．05）。Ⅲ组遮盖眼视网膜、脉络膜和巩膜RARβmRNA表达增强（P〈0．05）。结论去除形觉剥夺可以抑制近视。形觉剥夺眼视网膜RARβ蛋白的高表达早于屈光度和眼轴的改变。RARβ在形觉剥夺眼视网膜、脉络膜和巩膜中的表达增强。     

豚鼠形觉剥夺性近视眼后极部巩膜IGF-Ⅰ/IGF-ⅡmRNA的表达

目的目的观察豚鼠形觉剥夺性近视眼后极部巩膜IGF-Ⅰ/IGF-ⅡmRNA表达的变化,以探讨IGFs与形觉剥夺性近视发生的关系。方法实验用三色豚鼠30只,于出生后第2d,将左眼以半透明眼罩遮盖作为形觉剥夺眼,右眼不做任何处理为对照眼。测量实验前、遮盖4周、遮盖8周时遮盖眼和对照眼的屈光度、眼轴长度。遮盖8周实验结束时,RT-PCR检测后极部巩膜IGF-Ⅰ/IGF-ⅡmRNA的表达水平。结果形觉剥夺使遮盖眼后极部巩膜IGF-Ⅰ/IGF-ⅡmRNA表达升高,与对照眼相比差异有显著性意义（P〈0.05）。结论豚鼠巩膜可以自分泌/旁分泌IGF-Ⅰ、IGF-Ⅱ。形觉剥夺使遮盖眼后极部巩膜IGF-Ⅰ/IGF-ⅡmRNA表达升高,IGFs参与豚鼠形觉剥夺性近视形成中巩膜重塑的过程。     

鸡形觉剥夺性近视眼形态学及bFGF免疫组织化学研究

目的 了解形觉剥夺性近视（FDM）的参与因素。方法 实验鸡40只孵化2d，经初筛分为2组，切除实验组（右眼）上下睑缘各1mm，连续缝合，制造FDM的动物模型，遮盖时间为21d，常规视网膜检影法测屈光度，A型超声测眼轴长度，光学显微镜观察眼后极部组织病理变化，免疫组织化学法测后极部巩膜、视网膜中碱性成纤维细胞生长因子（bFGF）的变化。结果 诱发明显的FDM，实验眼眼轴延长（P〈0．05），镜下见实验眼巩膜软骨层增厚、纤维层变薄，软骨层内软骨细胞数目增多。bFGF免疫组织化学染色显示，bFGF在实验眼与对照眼巩膜、视网膜均有表达，在视网膜的表达实验眼强于对照眼，实验眼的视网膜外层又强于内层，巩膜bFGF的表达在两组间无显著性差异。结论 形觉剥夺性近视中有bFGF的参与。     

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。     

形觉剥夺性近视豚鼠巩膜形态学观察

目的观察形觉剥夺性近视豚鼠眼后极部巩膜的改变。方法4周龄豚鼠14只,随机分为正常对照组(Ⅰ组),形觉剥夺(FD)组(Ⅱ组)。Ⅱ组豚鼠右眼采用半透明眼罩遮盖的方法建立形觉剥夺近视模型,2周后检测其屈光度、眼轴长,并观察后极部巩膜组织的光镜、电镜改变。结果2周后剥夺眼屈光度相对于对照眼及年龄匹配对照组分别为-3.1 D±1.60 D,-3.2 D±1.72 D(P<0.01)。剥夺眼眼轴相对于对照眼(7.90 mm±0.13 mm、7.87 mm±0.17 mm,P<0.01)和正常眼(7.90 mm±0.13 mm、7.70 mm±0.16 mm,P<0.05)明显延长。剥夺眼后极部巩膜组织变薄,胶原纤维直径变小,纤维间空间增大。结论形觉剥夺刺激豚鼠眼巩膜组织变薄,其改变与人类近视巩膜组织改变相似。     

单眼形觉剥夺对豚鼠后极部巩膜整合素β1表达的影响

目的探讨豚鼠形觉剥夺性近视模型中巩膜整合素β1的表达及其与形觉剥夺的关系。方法40只出生后1周花色豚鼠,右眼遮盖作为形觉剥夺组,左眼不作处理作为对照组。遮盖2、4、8周和遮盖8周去遮盖1周后测量屈光度,眼科A超测定眼轴长度;对两组4个时间点眼球后壁行SP法免疫组织化学染色和RT-PCR检测巩膜整合素β1蛋白和mRNA水平的动态变化。结果与对照组相比,形觉剥夺组4个时间点眼球后壁巩膜整合素β1表达明显减少,差异有统计学意义（P〈0.05）,去遮盖1周后,表达上调,但仍低于对照组（P〈0.05）;而对照组间相比较,差异无统计学意义（P〉0.05）;形觉剥夺组和对照组屈光度、眼轴长度比较,差异有显著的统计学意义（P〈0.05）。结论豚鼠形觉剥夺时,后极部巩膜整合素β1表达减少,去遮盖后表达上调,提示整合素β1可能参与了形觉剥夺性近视的发生,其影响巩膜重塑的机制有待进一步研究。     

豚鼠实验性近视眼巩膜的羟脯氨酸含量改变

目的通过豚鼠形觉剥夺性近视眼巩膜羟脯氨酸含量的检测,分析形觉剥夺对豚鼠巩膜不同区域胶原的影响,探讨胶原水平的变化在哺乳类动物近视眼发生机制中的作用.方法出生3周的断乳花色雄性豚鼠24只,单眼眼睑缝合75d后,检影,测眼轴.后极和前部巩膜分别称重后,以蛋白酶K消化和盐酸水解,氯胺T氧化比色法测每毫克巩膜中的羟脯氨酸含量.结果豚鼠75d的形觉剥夺诱导了约-9D的相对近视和0.39mm的眼轴延长.剥夺眼前部巩膜和后极巩膜的羟脯氨酸含量有显著性统计学差异(P＜0.001);对照眼前后巩膜的羟脯氨酸含量无统计学差异(P＞0.05);双眼前部巩膜的羟脯氨酸含量差异无统计学意义(P＞0.05);双眼后部巩膜的羟脯氨酸含量差异有显著性(P＜0.001).结论豚鼠形觉剥夺性近视眼时,主要是后极部羟脯氨酸含量减少,即后极部的巩膜胶原优先受影响.由于后极部巩膜胶原减少,减弱了巩膜的抵抗力,使眼轴易于延展而发生近视.     

胰岛素样生长因子1受体反义寡核苷酸对豚鼠形觉剥夺性近视眼的抑制作用

目的观察豚鼠形觉剥夺性近视眼后极部视网膜胰岛素样生长因子1受体（insulin-like growth factor 1 receptor,IGF-1R）基因表达水平的动态变化,以及IGF-1R反义寡核苷酸玻璃体腔注射对形觉剥夺性近视眼屈光度及眼轴长度的影响,探讨视网膜IGF-1R在实验性近视眼发病中的作用。方法3周龄的三色豚鼠64只,随机均分为8组（每组8只）,A组：单眼遮盖7d;B组：未遮盖7d;C组：单眼遮盖14d;D组：未遮盖14d;E组：单眼遮盖14d后去遮盖7d;F组：未遮盖21d;G组：单眼遮盖14d＋玻璃体腔注射40μg（20μl）IGF-1R正义寡核苷酸;H组：单眼遮盖14d＋玻璃体腔注射40μg（20μl）IGF-1R反义寡核苷酸。检测各组的近视屈光度、眼轴长度以及后极部视网膜IGF-1R mRNA和蛋白质的表达水平。结果遮盖14d后实验眼眼轴明显延长,形成近视,去遮盖7d后,近视屈光度减低,眼轴增长减缓;随着遮盖时间的延长,后极部视网膜IGF-1R表达水平明显上调,去遮盖后,表达水平降低（P=0.000）。形觉剥夺14d后,IGF-1R正义寡核苷酸注射眼的眼轴长度 、近视屈光度以及后极部视网膜IGF-1R表达水平与单纯遮盖组无显著差异（P=0.664,0.797,0.312,0.117）;但IGF-1R反义寡核苷酸注射眼的近视屈光度显著减低,眼轴变短,后极部视网膜IGF-1R mRNA和蛋白质表达水平均明显下调（P=0.000）。结论形觉剥夺能上调豚鼠眼后极部视网膜IGF-1R的表达水平,去遮盖后,豚鼠近视屈光度减低,眼轴增长减缓,后极部视网膜IGF-1R的表达水平下调。利用反义寡核苷酸技术抑制视网膜IGF-1R基因的表达,可以抑制近视的发展。     

Recovery from axial myopia induced by a monocularly deprived facemask in adolescent (7-week-old) guinea pigs

PURPOSE: Guinea pigs have been increasingly used as an animal model for experimental myopia. Infant guinea pigs are susceptible to recovery from myopia within 2 weeks of form deprivation. This study investigated whether adolescent guinea pigs are susceptible to recovery from myopia after a longer period of form deprivation. METHOD: Twenty-two guinea pigs (age of 3 weeks) were randomly assigned to two groups: MDF (monocularly deprived facemask, n=11) and normal control (free of form deprivation, n=11). All animals underwent biometric measurement (refraction, corneal curvature and axial length) prior to the experiment. Animals in the MDF group wore a facemask that covered the right eye for 4 weeks. The MDF was then removed and biometric measurement was performed immediately and at 2, 6, 10 and 14 days. The same measurement was performed in the normal control group at time-points matching those of the MDF group. RESULTS: The MDF eyes were approximately 4D more myopic with a greater increase in vitreous length by 0.12 mm compared to either the fellow or the normal control eyes after form deprivation (p<0.01). This relative myopia shifted rapidly towards hyperopia within 2 days after removal of the MDF, followed by a more gradual recovery. A complete recovery occurred by 6 days after removal of the MDF compared to the fellow and normal control eyes (p>0.05). Vitreous length in the MDF eyes slightly reduced within 2 days after removal of the MDF and then remained steady. The MDF eyes were similar to both the fellow and normal control eyes in vitreous length (p>0.05) 6 days after removal of the MDF. There was no significant difference between the MDF, fellow and normal control eyes in the other axial components during the form deprivation and recovery period. CONCLUSION: Adolescent guinea pigs are susceptible to recovery from MDF-induced myopia. The refractive recovery is mainly correlated to the inhibited axial elongation of the vitreous chamber of the previously deprived eyes.     

Dynamic changes of ocular biometric parameters:a modified form-deprivation myopia model of young guinea pigs

AIM:To evaluate the dynamic ocular biometric changes of a modified form-deprivation myopia model in young guinea pigs.METHODS:The animals were randomly assigned to two groups:the monocularly deprived facemask group(MDF,with all the right eyes covered,n =24) and the normal control group(free of facemask,n =24).Each group was then equally divided into four subgroups which were followed up for 2,4,6 and 8 weeks,respectively.Parameters measured from every eye included refraction,corneal curvature,axial length and the dry weight of sclera at the posterior pole.RESULTS:All the facemasks remained in place during the follow-up.The covered eyes developed myopia with the vitreous chamber lengthening and the dry weight of posterior sclera reduced at each time point compared with the contralateral uncovered(P <0.05 at all time points).The changes had a linear correlation with the deprivation time(P <0.05).There were no significant differences in all the parameters between the uncovered eyes of MDF group and the normal control group(P >0.05 at all time points).CONCLUSION:Monocular form deprivation with the facemask is highly effective and non-invasive in inducing axial myopia in guinea pigs.The axial myopia is mainly caused by the increased vitreous chamber length and the weakened posterior sclera rigidity.The form-deprivation eye didn’t interfere with the natural development of the contralateral eye.     

Effects of 7‐methylxanthine on the sclera in form deprivation myopia in guinea pigs

Purpose: The aim of this study was to determine the effect of the adenosine receptor antagonist 7‐methylxanthine (7‐MX) on form deprivation myopia in 3‐week‐old guinea pigs. Methods: Two groups of 3‐week‐old guinea pigs were subjected to monocular deprivation (MD) using a diffuser and fed either 7‐MX (300 mg/kg body weight; n = 7) or vehicle control (saline at an equal volume to 7‐MX; n = 7). A control group (n = 6) was not subjected to form deprivation. Ocular refraction, axial length and body weight were measured at the start and after 21 days. The thickness of the posterior sclera was measured by light microscopy and the collagen fibril diameter in the inner, middle and outer layers of the sclera was measured by electron microscopy. Results: In the vehicle control group, 21 days of MD produced significant amounts of myopia, axial elongation, thinning of the posterior sclera and thinning of the median collagen fibril diameter in the posterior sclera relative to the contralateral eyes. In the guinea pigs fed with 7‐MX, however, form deprivation produced significantly less myopia and axial elongation compared with vehicle control animals. The 7‐MX‐treated animals exhibited a thickening of the posterior sclera in both the MD eye and the contralateral eye. In the 7‐MX‐treated animals, the median collagen fibril diameter in the posterior sclera was not reduced by form deprivation. Conclusions: Treatment with 7‐MX appears to not only decrease the amount of myopia by around 50% and eliminate the eye elongation induced by form deprivation in guinea pigs, but also to prevent form deprivation myopia‐related scleral changes, such as thinning of the sclera and thinning of the collagen fibril diameter in the posterior sclera.     

骨形态发生蛋白在形觉剥夺性近视眼后巩膜中表达的变化

背景眼球伸长过程伴随着巩膜的广泛重塑,而这种重塑受多种生长因子的调控。以往的研究证实转化生长因子-β（TGF-β）在近视形成和发展过程中发挥作用。骨形态发生蛋白（BMPs）属于TGF-β超家族,其在近视的发生中是否发挥作用及如何发挥作用尚不清楚。目的观察豚鼠形觉剥夺性近视（FDM）眼后巩膜中BMPs的表达变化,探讨其在近视后巩膜重塑中的作用。方法1～2周龄花色豚鼠30只,以随机数字表法随机分为实验组和正常对照组,每组15只。任意选择实验组豚鼠的一侧眼作为实验眼,应用半透明眼罩连续遮盖14d以建立FDM动物模型,另一侧眼作为对照眼。形觉剥夺前后所有动物眼经检影验光获得屈光度,用A型超声法测量眼轴长度。造模后第15天取豚鼠后巩膜组织,分别用逆转录PCR（RT—PCR）和Westernblot法检测各组豚鼠后巩膜中BMPsmRNA及其蛋白的表达。结果实验14d后,豚鼠遮盖眼的屈光度为（一0．48±0．51）D,与对侧眼的（3．22±0．34）D比较,差异有统计学意义（t=-12．814,P=0．000）,与正常对照眼的（2．97±0．70）D比较,差异有统计学意义（t=-11．878,P=0．000）。豚鼠遮盖眼的眼轴长度为（8．30±0．05）mm,明显长于对侧眼的（8．11±0．06）mm和正常对照组（8．06±0．06）mm,差异均有统计学意义（t=7．230、9．084,均P=0．000）。正常豚鼠后巩膜可表达BMP-2、BMP-4、BMP-5mRNA,豚鼠遮盖眼后巩膜中BMP-2mRNA和BMP-5mRNA的相对表达值分别为0．41-±0．11和0．65±0．06,较对侧眼的0．62-±0．07和0．84±0．03分别下降了34．48％和23．67％,差异均有统计学意义（t=2．838,P=0．017;t=2．524,P=0．028）;豚鼠遮盖眼后巩膜中BMP-2和BMP-5蛋白表达的相对值分别为0．44±0．06和0．70-±0．05,较对侧眼的0．61±0．05和0．824-0．03分别下降了23．42％和15．21％,差异均有统计学意义（t=2．465,P=0．030;t=2．445,P=0．031）,而形觉剥夺眼与对侧眼后巩膜中BMP-4mRNA及其蛋白相对表达量的差异均无统计学意义（mRNA：t=0．704,P=0．460;蛋白：t=0．987,P=0．365）。结论FDM眼后巩膜中BMP-2和BMP-5的表达下调,提示BMPs在实验性近视后巩膜重塑中可能发挥作用。     

豚鼠形觉剥夺超高度近视模型的形态学研究

目的建立豚鼠形觉剥夺超高度近视模型并观察其后极部各层组织的病理组织学变化。方法 2周龄三色豚鼠分为形觉剥夺组（12只）和非形觉剥夺对照组（8只）,于形觉剥夺前,形觉剥夺后4、6、10、14周分别对各组进行检影和眼轴性参数测量。通过病理组织学光镜检查分析形觉剥夺14周后各组视网膜、脉络膜和巩膜厚度及其形态学的变化。结果豚鼠形觉剥夺后随时间延长近视度数逐渐增高,10周后可达-10.00 D以上的超高度近视,14周后近视度数更高、个别个体可达-20.00 D。眼轴性参数相应延长。形觉剥夺超高度近视眼视网膜、脉络膜和巩膜较对照组均明显变薄并有病理性改变。结论应用遮盖法对豚鼠施行长期单眼形觉剥夺会形成超高度近视,10周后可达-10.00 D以上,超高度近视眼巩膜、脉络膜和视网膜明显变薄,脉络膜和巩膜结构发生紊乱。视网膜结构中感光细胞层变薄最为明显,推测其对超高度近视的发生起重要作用。     

透镜诱导性近视豚鼠生物参数及巩膜胶原含量的改变

目的探讨生物参数和巩膜胶原在透镜诱导性近视（LIM）发生发展过程中的变化及其机制。方法实验研究。选取3周龄英国种雄性三色短毛豚鼠36只,随机分为透镜诱导组（24只）和空白组（12只）。透镜诱导组右眼戴-10 D透镜诱导4周后进行检影验光和眼轴测量,并检测后极部和前部/赤道部巩膜干重、厚度,盐酸水解后检测2组相同面积后极部巩膜水解液中羟脯氨酸及氨基酸总量的改变。数据采用t检验分析。结果透镜诱导4周后豚鼠模型眼与对侧眼相比发生轴性近视（t=-14.90,P<0.01）,并伴有眼轴的明显延长（t=14.76,P<0.01）,差异有统计学意义,后极部巩膜干重和巩膜厚度较空白组均有明显降低（t=3.98、6.67,P＜0.01）,同时后极部氨基酸总量呈下调趋势（t=3.29,P＜0.01）。结论透镜诱导可以引起豚鼠玻璃体腔的延长、后极部巩膜干重减轻、厚度变薄、胶原合成减少等一系列改变,减弱了巩膜的抵抗力,使眼轴易于延展而发生近视。     

Dynamic changes of ocular biometric parameters: a modified form-deprivation myopia model of young guinea pigs

AIM: To evaluate the dynamic ocular biometric changes of a modified form-deprivation myopia model in young guinea pigs. METHODS: The animals were randomly assigned to two groups: the monocularly deprived facemask group (MDF, with all the right eyes covered, n=24) and the normal control group(free of facemask, n=24). Each group was then equally divided into four subgroups which were followed up for 2, 4, 6 and 8 weeks, respectively. Parameters measured from every eye included refraction, corneal curvature, axial length and the dry weight of sclera at the posterior pole. RESULTS: All the facemasks remained in place during the follow-up. The covered eyes developed myopia with the vitreous chamber lengthening and the dry weight of posterior sclera reduced at each time point compared with the contralateral uncovered(P<0.05 at all time points). The changes had a linear correlation with the deprivation time (P<0.05). There were no significant differences in all the parameters between the uncovered eyes of MDF group and the normal control group (P>0.05 at all time points). CONCLUSION: Monocular form deprivation with the facemask is highly effective and non-invasive in inducing axial myopia in guinea pigs. The axial myopia is mainly caused by the increased vitreous chamber length and the weakened posterior sclera rigidity. The form-deprivation eye didn't interfere with the natural development of the contralateral eye.     

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。     

透镜诱导豚鼠近视眼巩膜基质中基质金属蛋白酶2及其组织抑制剂和生长因子的变化

目的观察透镜诱导豚鼠近视眼巩膜基质中基质金属蛋白酶2（matrix metalloproteinases 2，MMP-2）、金属蛋白酶2组织抑制剂ftissue inhibitor of metaloproteinase 2，TIMP-2）和转化生长因子B2（transforming growth factorβ2，TGF—β2）和成纤维细胞生长因子（fibroblast growth factor，bFGF）的变化．探讨透镜诱导与形觉剥夺在近视眼发生机制上的异同点。方法 11只豚鼠于诱导前后分别验光、测量眼轴长度．用-6D的透镜诱导右眼作为诱导眼，左眼作为对照眼，诱导成功后，将豚鼠处死，摘除眼球，取后极部巩膜分别进行MMP-2和TIMP-2、TGF—β2和bFGF的免疫组织化学染色．观察它们在巩膜组织成纤维细胞胞浆中表达的阳性率和阳性细胞所占面积的百分比，并与对侧眼进行比较。结果11只豚鼠诱导眼成功诱导出（-3．31±1．04）D近视，诱导眼巩膜中MMP-2的阳性率为81．8％，对照眼为45．5％，差异有显著性；TIMP-2的阳性率36．4％，对照眼为72．7％；MMP-2染色阳性细胞面积百分比为0．22±0．15．对照眼为0．06±0．08（P〈0．05）；TIMP-2为0．05±0．08，对照眼为0．13±0．10。巩膜中TGF—β2阳性率为81．8％，对照眼为36．4％（P〈0．05），bFGF的阳性率为45．5％，明显低于对照眼（63．6％）。诱导眼TGF—β2染色阳性细胞面积百分比为0．21±0．14．对照眼为0．06±0．10，差异有显著性：bFGF为0．07±0．09，对照眼为0．15±0．14。结论透镜可以成功地诱导出豚鼠近视眼．透镜诱导近视眼巩膜基质中MMP-2活性增强，TIMP-2活性降低，TGF—β2表达增加，bFGF表达减少，MMP-2和TIMP-2、TGF—β2和bFGF之间存在平衡失调．它们的改变与形觉剥夺性近视的变化相似，表明透镜诱导近视眼与形觉剥夺性近视眼在巩膜基质的改变和生长因子的变化上存在相似的机制。