Immunochemical evidence for increased formation of advanced glycation end products and inhibition by aminoguanidine in diabetic rat lenses.
Immunochemical evidence for increased formation of advanced glycation end products and inhibition by aminoguanidine in diabetic rat lenses.
复制标题
糖尿病大鼠晶状体中晚期糖基化终产物形成增加和氨基胍抑制的免疫化学证据。
DOI：
10.1006/bbrc.1997.7744
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发表时间：
1997
影响因子：
3.1
通讯作者：
Abraham,EC
中科院分区：
文献类型：
--
作者：
Matsumoto,K;Ikeda,K;Horiuchi,S;Zhao,H;Abraham,EC
用cml特异性抗age单克隆抗体和抗age多克隆抗体对对照组和链脲霉素糖尿病大鼠的水溶性和尿素可溶性蛋白进行AGEs检测。糖尿病大鼠的AGEs，尤其是CML，显著增加，而氨基胍治疗导致AGEs显著降低。这些数据也证实了CML，一种糖氧化产物，是晶状体AGE结构的主要表位。
Water-soluble and urea-soluble protein fractions from control and streptozotocin-diabetic rats were analyzed for AGEs with a CML-specific monoclonal anti-AGE antibody and a polyclonal anti-AGE antibody. AGEs, CML in particular, were significantly increased in the diabetic rats whereas aminoguandine treatment resulted in significant decrease in AGEs. The data also confirm that CML, a glycoxidation product, is a major epitope of AGE structures in lenses.