用XIXA法对大鼠糖尿病性白内障锌含量改变的研究

在链脲佐菌素所致SD系大鼠糖尿病性白内障期间,用同位素激发X荧光分析(XIXA)法测定晶状体的Zn及K、Ca、Mn、Fe、Cu、Pb、Se等元素含量的改变。结果发现:在糖尿病性白内障的发病期间,Zn和Fe的含量显著增加;K含量显著降低;其他受检元素无显著变化。     

补锌对白内障大鼠晶状体NO和NOS的影响

目的 :探讨补锌对白内障大鼠晶状体中一氧化氮 (NO)和一氧化氮合酶 (NOS)的影响。方法 :用亚硒酸钠复制大鼠白内障模型 ,治疗组双眼点 0 4 %葡萄糖酸锌 (C12 H2 2 OM14 Zn)眼药水 ,对照组与模型组双眼不点任何眼药水。 10wk后观察各组实验大鼠晶状体的变化并测定晶状体中NO含量及NOS活性。结果 :白内障模型大鼠与对照组比较 ,晶状体NO含量和NOS活性差异均无显著意义 (P >0 0 5 ) ;治疗组晶状体NO含量和NOS活性与模型组和对照组比较 ,其差异无显著意义 (P >0 0 5 )。结论 :白内障大鼠眼内补锌对晶状体中NO含量和NOS活性没有明显影响     

老年性白内障血清、晶体及房水微量元素的测定

检测了部分老年性白内障房水,晶体及不同时期血清的13～33种元素的含量,结果表明:1.白内障晶体中Zn,K,As,P,Rb,Sb,Bi含量较透明晶体明显降低。Ca,Fe,Na,Li,Cr,Ba含量较透明晶体明显升高。2.随着白内障的发展,血清中Zn,Mg,Ti,Li,Si,Sn含量逐渐降低,白内障成熟时,血清中除Mg以外余者含量均降到最低,而Al的含量却逐渐升至最高,白内障成熟时Al的含量达到最高。3.白内障房水中Ca、K含量较透明晶体明显升高。上述结果表明,微量元素与白内障密切相关,可能是白内障的致病因素之一。     

白藜芦醇对糖尿病白内障大鼠正沉默信息调节因子2相关酶1基因表达的影响

目的  探讨白藜芦醇对糖尿病白内障大鼠晶状体正沉默信息调节因子2相关酶1（SIRT1）基因表达的影响。方法  80只Wistar大鼠随机分为4组：正常对照组、糖尿病模型组及白藜芦醇低剂量组及白藜芦醇高剂量组。糖尿病模型组、白藜芦醇低剂量组及白藜芦醇高剂量组一次性腹腔注射链脲菌素（STZ）（60 mg/kg）制备糖尿病大鼠模型。成模后低剂量组每日20 mg/kg,高剂量组每日100 mg/kg予白藜芦醇灌胃。裂隙灯显微镜照相机记录各组晶状体变化。12周实验结束时测定各组大鼠晶状体丙二醛（MDA）、超氧化物岐化酶（SOD）、谷胱甘肽过氧化酶含量。逆转录-聚合酶链反应（RT-PCR）检测各组大鼠晶状体SIRT1、肿瘤抑制因子P53、叉头转录因子1、核转录因子κB（NF-κB）表达情况。结果  糖尿病模型组大鼠晶状体均发生不同程度混浊,甚至完全混浊,形成白内障。白内障糖尿病大鼠晶状体MDA（7.96±0.51）nmol/mg·prot较正常对照组（4.21±0.27）nmol/mg·prot升高（P <0.01）,糖尿病白内障大鼠晶状体SOD、谷胱甘肽过氧化酶[（31.92±5.03）和（7.43±1.53）u/mg·prot]较正常对照组[（61.86±6.17）和（13.61±2.27）u/mg·prot]降低（P <0.01）。高剂量白藜芦醇组大鼠晶状体MDA（4.64±0.42）nmol/mg·prot较白内障糖尿病大鼠晶状体（7.96±0.51）nmol/mg·prot降低（P <0.01）。高剂量白藜芦醇组大鼠晶状体SOD、谷胱甘肽过氧化酶[（52.41±6.54）和（12.76±1.72）u/mg·prot]较白内障糖尿病大鼠晶状体SOD、谷胱甘肽过氧化酶[（31.92±5.03）和（7.43±1.53）u/mg·prot]增高（P <0.01）。白内障糖尿病大鼠晶状体SIRT1 mRNA表达（0.187±0.034）较正常对照组大鼠（0.523±0.089）降低（P < 0.01）。高剂量白藜芦醇组大鼠晶状体SIRT1 mRNA表达（0.497±0.072）较白内障糖尿病大鼠晶状体（0.187±0.034）增强（P <0.01）。白内障糖尿病大鼠晶状体P53、叉头转录因子1、NF-κB mRNA表达（0.816±0.153）、（1.269±0.231）、（0.896±0.029）较正常对照组（0.592±0.104）、（0.674±0.112）、（0.495±0.008）增强（P <0.01）。高剂量白藜芦醇组糖尿病大鼠晶状体P53、叉头转录因子1、NF-κB mRNA表达（0.609±0.107）、（0.713±0.121）、（0.397±0.018）较白内障糖尿病大鼠（0.816±0.153）、（1.269±0.231）、（0.896±0.029）降低（P <0.01）。结论  白藜芦醇可能通过调节SIRT1表达,进一步调节下游基因P53、叉头转录因子1、NF-κB的表达,抑制和延缓晶状体上皮细胞凋亡,延缓糖尿病大鼠白内障的发生发展。

     

Congenital Malformations in Experimental Diabetic Pregnancy: Aetiology and Antioxidative Treatment

Diabetes mellitus in pregnancy causes congenital malformations in the offspring. The aim of this work was to characterize biochemical and morphologic anomalies in the conceptus of an animal model of diabetic pregnancy. In addition, a preventive treatment against diabetes-induced dysmorphogenesis was developed.

Congenital cataract was often found in the offspring of diabetic rats. The fetal lenses had increased water accumulation, sorbitol concentration and aldose reductase activity compared to control lenses. The results suggest that the cataracts form via osmotic attraction of water due to sorbitol accumulation in the fetal lens.

Another set of malformations, with possible neural crest cell origin, occurred frequently in offspring of diabetic rats. These included low set ears, micrognathia, hypoplasia of the thymus, thyroid and parathyroid glands, as well as anomalies of the heart and great vessels. Furthermore, diabetes caused intrauterine death and resorptions more frequently in the late part of gestation.

When the pregnant diabetic rats were treated with the antioxidants butylated hydroxytoluene, vitamin E or vitamin C., the occurrence of gross malformations was reduced from approximately 25% to less than 8%, and late resorptions from 17% to 7%. This suggests that an abnormal handling of reactive oxygen species (ROS) is involved in diabetes-induced dysmorphogenesis in vivo. Indeed, an increased concentration of lipid peroxides, indicating damage caused by ROS, was found in fetuses of diabetes rats. In addition, embryos of diabetic rats had low concentrations of the antioxidant vitamin E compared to control embryos. These biochemical alterations were normalized by vitamin E treatment of the pregnant diabetic rats.

The antioxidants are likely to have prevented ROS injury in the embryos of the diabetic rats, in particular in the neural crest cells, thereby normalizing embryonic development. These results provide a rationale for developing new anti-teratogenic treatments for pregnant women with diabetes mellitus.     

阿司匹林滴眼液防治糖尿病性白内障

目的:探讨阿司匹林滴眼液抑制糖尿病性白内障的作用效果及作用机制.方法:复制链脲佐菌素(streptozocin, STZ)糖尿病大鼠模型,成模后(血糖＞14 mmol/L)将动物分为低浓度阿司匹林治疗组(0.5 g/L)、高浓度阿司匹林治疗组(1 g/L)和未治疗组.治疗组每日给予2次阿司匹林滴眼液治疗左眼,采用裂隙显微镜观察并记录晶状体混浊的程度,使用分光光度计测定晶状体中谷胱甘肽、糖基化终末产物(advanced glycation end product, AGE)的含量以及谷胱甘肽还原酶、过氧化氢酶的活性.结果:建立糖尿病大鼠模型后6至9 wk,与糖尿病大鼠相比,治疗组大鼠晶状体混浊程度降低0.5～1个级别,谷胱甘肽的含量升高20%,过氧化氢酶的活性增强260%,而AGE的含量降低28%,它们之间差异均具有统计学意义(P＜0.05).结论:阿司匹林可能通过抑制晶状体蛋白质糖基化和氧化损伤的综合作用,延缓早期的糖尿病大鼠晶状体混浊.     

用‘H—NMR谱对大鼠糖尿病性白内障和正常晶状体山梨醇...

The pulse Fourier NMR was employed to measure the artificial diabetic cataract lens at various stages of its formation, and the lenses of the normal rats. Data obtained by using this method show that all the peaks that of water concentrate in the range of delta less than 4 ppm. The peak value at delta = 3.20 ppm is on a marked increase during the formation of cataract which is caused by the phosphate metabolites, such as GPC, ATP, ... etc, in cataract lens. With the development of the disease, the peak width at delta = 3.73 ppm becomes greater and greater, which shows that the activity of sorbitol dehydrogenase has decreased. This leads to a high concentration of the sorbitol in the cataract lens. Consequently, the osmosis pressure in the cataract lens is increased, and excessive water might dip into the crystalline lens to keep the balance of the osmosis pressure. And this might result in the hydration of the fiber cell of the crystalline lens, which might cause a swelling or blisters. These results are in favour of the prolongation of the relaxation time of cataractous lens reported in our other papers, and also support those gained by biochemical studies issued in the medical literature.     

水通道蛋白在大鼠氧化性白内障晶状体上的表达

目的 观察Ⅰ型水通道蛋白（AQP1）在正常及氧化性白内障模型大鼠晶状体上的表达，探讨其在氧化性白内障发生过程中的作用。方法 将健康清洁级Wistar大鼠60只离体透明晶状体随机分为2组，实验组加2mmol／L H2O2，空白组不加H2O2，其余处理相同。分别于12、24及48h观察两组大鼠晶状体的混浊情况；运用免疫组织化学方法及计算机图像分析技术检测AQP1的表达。结果 加入培养液后48h，空白组晶状体透明，而实验组的晶状体有不同程度的混浊；实验组晶状体的AQP1表达较空白组少，差异有显著性意义（P〈0．05）。结论 AQP1的减少在氧化性白内障的发生中有一定作用，氧化损伤可能通过减少AQP1在晶状体上皮细胞膜上的表达，影响晶状体囊膜水代谢，以诱发白内障。     

糖尿病性白内障围术期临床分析

目的探讨糖尿病性白内障围术期的合理处理方法。方法回顾性分析108例（120眼）糖尿病性白内障手术患者的临床资料。结果108例（120眼）患者中伤口Ⅰ期愈合107例（119眼），1例（1眼）出现严重感染，行眼内容摘除术，8例（9眼）人工晶体前膜形成。术后1周视力≥0．576例。结论正确把握糖尿病白内障手术时机，重视血糖检查在白内障手术中的重要性，才能提高疗效，降低糖尿病眼病的致盲率。     

转化生长因子β1和基质金属蛋白酶2在糖尿病性白内障大鼠晶状体上皮细胞中的表达及意义

目的 探讨糖尿病性白内障大鼠晶状体上皮细胞(lens epithelial cells,LECs)中转化生长因子β1(transforming growth factor β1,TGF-β1)和基质金属蛋白酶2(matrix metalloproteinase-2,MMP-2)的表达情况及其意义。 方法 将28只SD大鼠随机分为白内障组和对照组,建立糖尿病性白内障大鼠模型,观察2组大鼠LECs变化,测定2组大鼠LECs中TGF-β1和MMP-2表达情况。 结果 HE染色:白内障组大鼠LECs形态异常,排列紊乱,核大小不均匀,胞质疏松;对照组大鼠LECs正常。白内障组大鼠2周末和4周末LECs中TGF-β1蛋白和MMP-2蛋白平均光密度(0.045±0.002、0.075±0.006;0.028±0.003、0.055±0.006)均高于对照组(0.006±0.001、0.006±0.002;0.000、0.000,均P＜0.05),白内障组大鼠4周末LECs中TGF-β1蛋白和MMP-2蛋白平均光密度高于2周末(P＜0.05)。白内障大鼠LECs中TGF-β1蛋白和MMP-2蛋白呈正相关(r=0.915,P=0.004)。 结论 糖尿病性白内障的发生发展可能和LECs中TGF-β1蛋白、MMP-2蛋白水平升高有关,糖尿病性白内障LECs中TGF-β1蛋白和MMP-2蛋白呈正相关。