Kobayashi T
Department of Ophthalmology, Koshigaya Hospital, Dokkyo University School of Medicine, Japan.
Nippon Ganka Gakkai Zasshi. 2000 May;104(5):306-11.
Molecular features of lipoprotein(a) [Lp (a)] associated with membranes of the lens were examined with respect to the pathogenesis and progression of cataract.
Lenses were homogenized and separated into urea-soluble (US) and water-soluble (WS) fractions. Then low density lipoprotein (LDL) and high density lipoprotein (HDL) fractions were separated from US & WS fractions by flotation density gradient ultracentrifugation. LDL and HDL fractions were prepared from 14 and 54 lenses, respectively, of a group of diabetic patients with senile cataract (DM group) or a group of non-diabetic patients with senile cataract (non-DM group). Lp(a) in each fraction and in human aqueous humor was immunochemically assayed using the latex agglutination method. Molecular phenotypes of Lp(a) were identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) followed by western blotting.
Lp (a) contents in LDL fractions were significantly higher (p < 0.05) in the DM group [11.14 +/- 0.88(mean +/- standard deviation) micrograms/lens] than in the non-DM group [5.77 +/- 2.75 micrograms/lens]. Lp(a) values in HDL fractions were higher in the DM group than in the non-DM group, although the values did not differ significantly between the two groups. Lp (a) concentration in aqueous humor was slightly higher in the DM group than in the non-DM group. Lp (a) components examined by SDS-PAGE were detected only at the origin using immunoblotting.
The Lp(a) content in cataractous lenses was higher in the DM group than in the non-DM group. In contrast to the molecular features of Lp(a) in blood, those of Lp(a) in cataractous lens seemed to be high molecular weight complexes. These results suggests that impairment of LDL receptors in DM is associated with disturbance in lipid metabolism which leads to accumulation of degenerated lipoproteins and altered membrane structure.
就白内障的发病机制和进展情况,对与晶状体膜相关的脂蛋白(a)[Lp(a)]的分子特征进行研究。
将晶状体匀浆并分离为尿素可溶性(US)和水溶性(WS)部分。然后通过浮选密度梯度超速离心从US和WS部分中分离出低密度脂蛋白(LDL)和高密度脂蛋白(HDL)部分。分别从一组患有老年性白内障的糖尿病患者(糖尿病组)或一组患有老年性白内障的非糖尿病患者(非糖尿病组)的14只和54只晶状体中制备LDL和HDL部分。使用乳胶凝集法对每个部分以及人房水中的Lp(a)进行免疫化学分析。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)然后进行蛋白质印迹来鉴定Lp(a)的分子表型。
糖尿病组LDL部分中的Lp(a)含量[11.14±0.88(平均值±标准差)微克/晶状体]显著高于非糖尿病组5.77±2.75微克/晶状体。糖尿病组HDL部分中的Lp(a)值高于非糖尿病组,尽管两组之间的值没有显著差异。糖尿病组房水中的Lp(a)浓度略高于非糖尿病组。通过SDS-PAGE检测的Lp(a)成分在免疫印迹中仅在原点处被检测到。
糖尿病组白内障晶状体中的Lp(a)含量高于非糖尿病组。与血液中Lp(a)的分子特征相比,白内障晶状体中Lp(a)的分子特征似乎是高分子量复合物。这些结果表明,糖尿病患者LDL受体的受损与脂质代谢紊乱有关,脂质代谢紊乱会导致变性脂蛋白的积累和膜结构的改变。