中文摘要：

目的 探讨人突变Lumican基因转基因小鼠形觉剥夺性近视模型的眼球生物学参数的变化,比较人Lumican基因突变与形觉剥夺对小鼠眼轴、屈光度数及巩膜发育的影响.方法 实验研究.由50只人突变Lumican基因转基因鼠（10日龄）中随机选取34只,以及46只同日龄野生C57BL/6J小鼠中随机选取32只,以眼睑缝合法建立单眼形觉剥夺模型,其余转基因小鼠（16只）及野生鼠（14只）不作处理.依据眼别将其分为6组：转基因小鼠未处理组（A组,16只,32只眼）;转基因小鼠形觉剥夺眼组（B组,34只,34只眼）;转基因小鼠形觉剥夺对侧眼组（C组,34只,34只眼）;野生小鼠未处理组（D组,14只,28只眼）;野生小鼠形觉剥夺眼组（E组,32只,32只眼）;野生小鼠形觉剥夺对侧眼组（F组,32只,32只眼）.各组小鼠8周龄（56日龄）时经复方托吡卡胺散瞳后行检影验光,测量双眼屈光度数,并以等效球镜度数表示.脱颈法处死小鼠后摘取眼球组织,行离体眼轴测量,后分离巩膜组织,实时荧光定量PCR（qPCR）技术于RNA水平上检测各组样本巩膜组织中Lumican基因表达情况.采用单因素方差分析联合LSD检验比较转基因小鼠与野生小鼠中形觉剥夺眼、对侧眼和未处理眼的基因水平表达量、屈光度及眼轴结果,转基因小鼠与野生小鼠间比较采用两独立样本t检验进行统计学分析.结果 巩膜组织中Lumican基因表达量在转基因小鼠形觉剥夺眼中表达增加,较对侧眼及未处理眼差异具有统计学意义（F=6.262;P＜0.05）;转基因小鼠形觉剥夺眼、对侧眼较野生小鼠相应眼表达也明显增加,差异具有统计学意义（t=4.772,2.218;P＜0.05）.形觉剥夺46 d后,转基因小鼠和野生小鼠形觉剥夺眼屈光度分别为（-0.38±1.10）和（0.14±1.26）D,相对于对侧眼及未处理眼差异有统计学意义（F=9.525,10.067;P＜0.01）;平均眼轴长度分别为（3.28±0.07）和（3.24±0.09） mm,

英文摘要：

Objective To investigate ocular changes in the monocularly deprivation myopic model of mutant Lumican transgenic mice.Comparing influences on biological parameters and sclera development between Lumican transgenic and form deprivation mice,and to prepare for further study of pathogenesis of pathological myopia （PM）.Methods Experimental research.Lumican transgenic mice and wild mice were monocularly lid-sutured at ten days after birth.All eyes were divided into 6 groups,group A（32 eyes）：control eyes in transgenic mice;group B（34 eyes）：sutured eyes in transgenic mice;group C（34 eyes）：fellow eyes in transgenic mice;group D（28 eyes）：control eyes in wild mice;group E（32 eyes）：sutured eyes in wild mice;group F（32 eyes）：fellow eyes in wild mice.Refraction was measured by streak retinoscopye and axial length was measured by vernier caliper at 8 weeks （56 days） after birth.Lumican expression was detected by quantitative real-time PCR in all groups.Results The refraction in group B and group E were （-0.38±1.10） D and （0.14± 1.26）D respectively,which were significantly different compared with contralateral groups and normal control groups （F=9.525,10.067;P〈0.01）.The mean axial length were also increased in group B （（3.28 ±0.07）mm and group E （3.24±0.09）mm,（F=7.183,6.671;P〈0.05）.Expression level of Lumican mRNA in sclera was increased in group B,which was significantly different from group A and group C （F=6.262;P〈0.05）.The expression of Lumican mRNA was increased in group B and C when compared with group E and F （t=4.772,2.218,P〈0.05）.Conclusions Form-deprivation in mutant Lumican transgenic mice causes myopic changes in deprived eyes.The gene expression level of Lumican in sclera of transgenic mice is significantly increased compared with contralateral eyes or that of wild group.Lumican mutation may effect the development of PM,and the interaction of genetic and environmental factors may lead to development of PM.